Phospho-NF-kB p65 (Ser536) Antibody | Affinity Biosciences LTD|亲科生物官网

$Figure 5.| Analysis of signaling pathways. (A) Protein levels of NF‑κB P65, p‑P65, IKKβ and IκBα in the total cell fraction of control and co‑cultured Jurkat cells and (B) densitometric analysis of the western blot data.$

Figure 5.

FIGURE 4| Overexpression of uc.

Figure 4.

Fig.

FIGURE 5|BB abrogates the activation of NFκB pathway in the testis of DM rats.

FIGURE 7 | Effects of Huangqin decoction (HQD) on colonic expression levels of nuclear factor-kappa B (NF-kB) pathway proteins assessed by Western blot in dextran sulfate sodium (DSS)-induced colitis mice (A).

Supplemental Figure 7.

FIGURE S3 | miR-26a-overexpressing exosomes exert a similar effect as an NF-κB inhibitor in promoting axonal regeneration and inhibiting astrogliosis.

Fig.

FIGURE 9 | p65 phosphorylation at Ser536 is suppressed by HSV-1 UL2.

Fig.

Figure 6.

Fig.

Figure 7 Eriodictyol-induced apoptosis of glioma cells is mediated by the PI3K/Akt/NF-κB signaling pathway.

Figure 6 CD47 deficiency promotes HFD-induced nuclear factor-κB (NF-κB) activation and translocation.

Fig.

Figure 7 The effect of etanercept on the expressions of TRAF2, p38, P-p38, p65, P-p65 in B cells stimulated by BAFF and TNF-α.

Fig.

FIGURE 7 NF-κB/TWIST1 mediates the effect of S.

Fig.

Figure 2 Analysis of Interested Molecular Expression in Breast Tumor Tissues of Patients (A) Relative expression of miR-7, ESAM, and RELA were analyzed in breast tumor tissues and adjacent normal tissues of 12 patients by qRT-PCR.

Fig.

Figure 6.

Fig.

FIGURE 4 The deficiency of Smad4 inhibited the inflammatory response in a cellular model of human insulin resistance.

Figure 3.

Fig.

FIGURE 4 Expression of ANX‐A1 (37 kDa), p‐NF‐κB p65, ICAM‐1, TNF‐α and IL‐1β.

Fig.

Figure 3 Treatment with HP promotes apoptosis of Dami cells through the NF-κB/IL-17 pathway.

FIGURE 8 Effects of OCOP and COP on the NF-κB pathway in DSS-induced mice (A) Representative Western blotting images of pIκBα, IκBα, cytoplasmic p65 and nuclear p65 (B–E) The protein expression levels of pIκBα, IκBα, cytoplasmic p65 and nuclear p65 in the NF-κB pathway.

Figure 3 Nampt promoted LPS-induced inflammation in MC3T3-E1 cells.

Figure 5 Tumor necrosis factor-induced protein-8 (TIPE)-mediated activation of the PI3K/Akt pathway is involved in the modulation of DcR3 levels in HCT116 cells.

Figure 8 Inhibition of TLR4/MAPK/NF-κB signaling pathway.

Figure 3 AOPPs reduced phosphorylation of Akt and promoted the phosphorylation of P65.

Fig.

Figure 5.

Figure 6 BE-BJO inhibited the activation of the NF-κB signaling pathway.

Figure 5 Bovine miR-125b regulates the expression of NF-κB, TNF-α and IL-6 in LPS-induced MAC-T cells.

Figure 5 Electroacupuncture pretreatment ameliorates HMGB1 and phosphor-NF-κB expression in the microglia.

Fig.

Figure 4.

Figure 6 |C-PC treatment suppresses the expression of NLRP3 inflammasome and NF-κB signaling pathway in lung tissues.

FIGURE 2 | Effects of the RvE1 and LXA4 combination on NF-κB modification.

Fig.

Figure 5 Rosiglitazone attenuates bone cancer pain (BCP) through the activation of proliferator-activated receptor-γ (PPAR-γ) to inhibit the nuclear factor-kappa B (NF-κB)/nod-like receptor protein 3 (NLRP3) inflammatory axis in spinal cord neurons.

Fig.

Figure 4 Effects of Y-1 and Y-2 on NRK-52e cells’ inflammatory cytokines stimulated by sodium oleate with/without CD36 silences representative.

Figure 8.

FIGURE 4| The deficiency of Smad4 inhibited the inflammatory response in a cellular model of human insulin resistance.

FIGURE 9 Effects of PAR-1 knockdown on p-NF-κB p65 by western blot (a) as well as NF-κB p65 (b) and p-NF-κB p65 (c) by immunofluorescence in SH-SY5Y cells treated with high glucose.

Figure 4 Effects of KDM2B on TLR4, NF-κB p65 and NLRP3 expression levels in myocardial ischemia-reperfusion injury in rats.

Figure 10 RBFOX1 affects the NF-κB and NRF2/HO-1 pathway in H/R-induced HK-2 cells.

Fig.

Figure 6.

Fig.

FIGURE 2 Punicalagin suppresses the TNF-α and IL-17A-induced IL-1β upregulation via inhibiting NF-κB activation and cleaved caspase-1 expression in vitro.

Figure 5.

$Figure 8 Curcumin relieved LPS-induced sepsis. (A) After the last 4-OHT injection, Rosa26LSL-MLS-Stat3 and Rosa26LSL-MLS-Stat3;UbcERT2Cre/+ mice were injected with curcumin prior to LPS. Survival was monitored every 6 - 12 h after injection. The data shown represent a combination of two independent experiments. Statistical comparison of survival was performed with a log-rank test. **, P < 0.01, *, P < 0.05. (B) Serum samples were obtained from these mice and subjected to ELISA to examine MCP-5 levels. (C-D) The serum levels of LDH and albumin were assessed. (E) Lung tissues were removed, and the percentages of macrophages were analyzed by flow cytometry. (B-E) The data are representative of one of two independent experiments. Significance was calculated using a two-way ANOVA. **, P < 0.01, * P < 0.05, n.s., not significant. (F) Rosa26LSL-MLS-Stat3 and Rosa26LSL-MLS-Stat3;LyzCre/+ mice were injected with 10 mg/kg curcumin prior to LPS (20 mg/kg). Survival was monitored every 6 - 12 h after injection. Statistical comparison of survival was performed with a log-rank test. **, P < 0.01, *, P < 0.05. (G) BMDMs of the indicated genotypes were treated with 8 μM curcumin for 20 h and incubated with either 100 ng/mL LPS (30 min) or 100 ng/mL IFN-α (1 h) before harvesting. The cells were harvested, lysed, and subjected to a Western blot analysis. The membranes were blotted with the indicated antibodies. (H) Cells were treated with 8 μM curcumin for 20 h and incubated with 100 ng/mL LPS for another 15 min. Nuclei and cytoplasmic fractions were extracted. The levels of the indicated proteins were analyzed by a Western blot analysis. (I) BMDMs were treated with curcumin. After 20 h, these cells were stimulated with or without 100 ng/mL LPS for 6 h before loading. BMDMs were then treated sequentially with BSA-conjugated palmitate, oligomycin, FCCP, and ETO as indicated. The data are representative of one of two independent experiments performed with n = 5. (J) 4-OHT-treated BMDMs were treated with curcumin for 20 h, and then, the BMDMs were exposed to 100 ng/mL LPS and 10 μmol/L MG132 for an additional 6 h before harvesting. The cell lysates were isolated, IP with an anti-CPT1a antibody and analyzed by a Western blot analysis using an anti-ubiquitin antibody. (G, H and J) The results shown are representative of one of three independent experiments. (K) Schematic representation of the mitochondrial STAT3-mediated increase in FAO in a USP50-dependent manner in the LPS-induced sepsis model. Upon the LPS stimulation, mitochondrial STAT3 could induce CPT1a stabilization by promoting USP50 expression and facilitating CPT1a-USP50 binding, leading to a switch from glucose to an increased reliance on FAO for ATP production, which, in turn, further enhanced NF-κB nuclear localization, leading to a great amount of cytokine production.$

Figure 8 Curcumin relieved LPS-induced sepsis.

Fig.

Figure 4 Effect of MG activated CAP-SIRT1 pathway on NF-κB-mediated inflammatory response in rat macrophages.

Fig.

Figure 6 Curculigoside treatment alleviated osteoclast-associated gene expression in Ti-induced BMSCs.

Fig.

FIGURE 3.

Figure 5 WKYMVm inhibited the ERK1/2 and NF-κB p65 signaling pathways and affected the p38 signaling pathway in microglial cells.

Fig.

FIGURE 6 Superoxide dismutase (SOD)@zeolite imidazolate framework-8 (ZIF-8) administration counteracted inflammation in the cochlea caused by noise exposure.

Figure 6 Effect of irisin on IL-1β-induced activation of NF-κB signaling in SW1353 cells.

Figure 6 Gal-3 inhibition reduced diabetes-induced macrophage infiltration and NF-κB p65 activation.

FIGURE 4 Cytoplasmic mtDNA markedly activated STING signalling.

Fig.

FIGURE 7 Nesfatin‐1 prevented activation of NF‐κB signaling in SCI mice.

Figure 5 The expression degrees of HMGB1, TLR4, NF-κB, p-38 MAPK, and ERK1/2 proteins (x¯ ±s).

Figure 7 The effect of OBB on the TLR4/NF-κB signaling pathway in 5-FU-induced IM mice.

Fig.

Figure 4 The expression of inflammatory proteins in pneumonia mice after SH treatment.

Figure 7 XFZYD inhibited the IKBα/NF-κB signaling in rat models with CPB-induced ALI.

Fig.

Figure 4 Berberine regulated the expression of phosphorylated NF-κB and Nlrp3 in mice with ALI.

Figure 7 BA improved the expressions of MYD88, p–NF–κBp65/NF-κBp65, p-IκBa/IκBa, TLR2, and TLR4 in rat lung tissue.

Figure 4 mRNA and protein expression in knee joint and spleen of CIA rats.

Figure 2 The NOD1/NF-κB signaling pathway was activated in the liver of piglets challenged with LPS.

Fig.

Figure 4 The BGF effects on levels of oxidative stress-related factors and inflammasome factors.

Fig.

Figure 2 chTERT activated the NF-κB signaling pathway.

Fig.

Figure 4.

Figure 5 Effect of MALT1 mucosa-associated lymphoid tissue lymphoma translocation protein 1 on nuclear factor-κB signaling in proatherogenic VSMCs.

Figure 7 SHFM1 regulates the NF-κB signaling pathway in ESCC cells.

Figure 5 Relative expression levels of NF-κB pathway-related proteins were measured via western blot assay.

Fig.

FIGURE 4 Ox‐LDL/LPS activated ADAM17 to increase cleavage of mTIMD4 in macrophages.

Figure 4 XNJY regulates the NF-κB/IκB-α pathway in PSD model rats.

Figure 2 Gla ameliorated liver inflammation induced by ethanol via activating the NF-κB pathway in vivo.

Figure 6 HSP90AA1 over-expression activates STAT1 and P65 in PK-15 and 3D4/2 cells.

Figure 5.

Figure 4 GALNT6 promotes the release of inflammatory factors and pyroptosis in PDAC cells.

Figure 3 Expression of regulated on activation, normal T-cell expressed and secreted protein in Caco2 cells in each group.

Fig.

Figure 4.

Fig.

Figure 7 Upregulated expression of TRAF6/NF-κB/HIF-1α/VEGF pathway in HPH that aggravated by Cul 5 further (A) The effect of hypoxia treatment for 4 weeks on Cul5/TRAF6/NF-κB/HIF-1α/VEGF pathway expression in lung tissues of mice, and reverse effect of pevonedistat.

Fig.

Figure 4 Effects of AdipoRon on p65 and adenosine monophosphate-activated protein kinase (AMPK) phosphorylation under proinflammatory conditions.

Fig.

Figure 8 Western blot analysis of the proteins.

Fig 4 miR-328-3p affects the expression of NF-κB signaling pathway and inflammation-related molecules after OGD treatment.

Fig 3 HEX enhances barrier integrity and limits the NF-κB signaling pathway in MMECs.

Figure 9.

Fig.

Figure 4 High-dose VC attenuated the inflammatory response in CLP-induced sepsis rats at 1d, 3d and 5d.

Figure 3 OR11H1‐A63 increased GADD45G expression and activated the NF‐κB and MAPK pathways.

Figure 6 BA alleviates pyroptosis and inflammation in the spinal cord tissue of SCI rats.

Fig.

Figure 6 Luteolin inhibits the activity of the AGE-RAGE signaling pathway.

Fig.

$Figure 2. ASFV A528R inhibits the NF-κB p65 phosphorylation downstream TLR8 signaling. (A) 293T cells grown in 12-well plate (3 × 105 cells/well) were transfected with A528R plasmid (0.25 µg, 0.5 µg), pTLR8 (0.5 µg) as indicated. Twenty-four hours post transfection, cells were stimulated with R848 (5 µg/mL) for 12 h, the expressions of p-p65, p65, A528R, and pTLR8 were analyzed by Western blotting. (B–D) 293T cells were transfected with A528R (0.25 µg, 0.5 µg) or vector (EV) control (0.5 µg), together with MyD88 (0.5 µg) (B), IKK-β (0.5 µg) (C), p65 (0.5 µg) (D). Twenty-four hours later, the expressions of p-p65, p65, A528R, MyD88, IKK-β, p65 were analyzed by Western blotting. (E) 293T cells grown in 12-well plate (3 × 105 cells/well) were transfected with A528R (0.25 µg, 0.5 µg), pTLR8 (0.5 µg). Twenty-four hours post transfection, cells were stimulated with R848 (5 µg/mL) for 12 h. Cell lysates were fractionated into cytoplasmic and nuclear extracts, and the protein levels of p65 and p-p65 in different fractions were analyzed by Western blotting. The histone-H3 and GAPDH were also shown as the nuclear and cytoplasmic markers, respectively.$

Figure 2.

Figure 7 Pretreatment with CH223191 eliminated the blocking effect of 5-HIAA on NF-κB signaling pathway The expression levels of representative proteins of the NF-κB pathway in mammary (A) and colonic (D) tissues were determined in three groups of mice.

产品:	磷酸化 NF-kB p65 (Ser536) 抗体
货号:	AF2006
描述:	Rabbit polyclonal antibody to Phospho-NF-kB p65 (Ser536)
应用:	WB IHC IF/ICC IP
反应:	Human, Rat, Monkey
预测:	Mouse, Pig, Bovine, Horse, Sheep, Dog
分子量:	65 kDa; 60kD(Calculated).
蛋白号:	Q04206
RRID:	AB_2834435

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阻断肽(封闭肽)是特异性结合目标抗体和阻断抗体结合的多肽。这些多肽包含抗体识别的抗原表位。与阻断肽结合的抗体不再与靶蛋白上的表位结合。例如，在免疫印迹(WB)和免疫组化(IHC)中，通过比较被阻断抗体和未阻断抗体的染色，可以看到哪种染色是特异性的。

规格	价格	库存
50ul	RMB¥ 1300	现货
100ul	RMB¥ 2400	现货
200ul	RMB¥ 3200	现货

货期: 当天发货

联系销售

MSDS

说明书

COA

实验方案

WB Handbook

IHC Protocol

IF/ICC Protocol

产品描述

来源:

Rabbit

应用:

WB 1:500-1:2000, IHC 1:50-1:500, IP 1:100-1:500, IF/ICC 1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:

Human,Rat,Monkey

预测:

Mouse(%), Pig(100%), Bovine(91%), Horse(91%), Sheep(91%), Dog(100%)

克隆:

Polyclonal

特异性:

Phospho-NF-kB p65 (Ser536) Antibody detects endogenous levels of NF-kB p65 only when phosphorylated at Serine 536.

RRID:

AB_2834435
引用格式: Affinity Biosciences Cat# AF2006, RRID:AB_2834435.

偶联:

Unconjugated.

纯化:

The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.

保存:

Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, sodium azide and glycerol. Store at -20 °C. Stable for 12 months from date of receipt.

别名:

展开/折叠

Avian reticuloendotheliosis viral (v rel) oncogene homolog A; MGC131774; NF kappa B p65delta3; NFKB3; Nuclear Factor NF Kappa B p65 Subunit; Nuclear factor NF-kappa-B p65 subunit; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3; OTTHUMP00000233473; OTTHUMP00000233474; OTTHUMP00000233475; OTTHUMP00000233476; OTTHUMP00000233900; p65; p65 NF kappaB; p65 NFkB; relA; TF65_HUMAN; Transcription factor p65; v rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B cells 3 (p65)); V rel avian reticuloendotheliosis viral oncogene homolog A; v rel reticuloendotheliosis viral oncogene homolog A (avian); V rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B cells 3, p65;

抗原和靶标

免疫原:

Uniprot:

Q04206(TF65_HUMAN) >>Visit HPA database.

基因/基因ID:

RELA(5970)

描述:

NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA, or RELB (MIM 604758) to form the NFKB complex. The p50 (NFKB1)/p65 (RELA) heterodimer is the most abundant form of NFKB. The NFKB complex is inhibited by I-kappa-B proteins (NFKBIA, MIM 164008 or NFKBIB, MIM 604495), which inactivate NFKB by trapping it in the cytoplasm.

序列:

Q04206 TF65_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

MDELFPLIFPAEPAQASGPYVEIIEQPKQRGMRFRYKCEGRSAGSIPGERSTDTTKTHPTIKINGYTGPGTVRISLVTKDPPHRPHPHELVGKDCRDGFYEAELCPDRCIHSFQNLGIQCVKKRDLEQAISQRIQTNNNPFQVPIEEQRGDYDLNAVRLCFQVTVRDPSGRPLRLPPVLSHPIFDNRAPNTAELKICRVNRNSGSCLGGDEIFLLCDKVQKEDIEVYFTGPGWEARGSFSQADVHRQVAIVFRTPPYADPSLQAPVRVSMQLRRPSDRELSEPMEFQYLPDTDDRHRIEEKRKRTYETFKSIMKKSPFSGPTDPRPPPRRIAVPSRSSASVPKPAPQPYPFTSSLSTINYDEFPTMVFPSGQISQASALAPAPPQVLPQAPAPAPAPAMVSALAQAPAPVPVLAPGPPQAVAPPAPKPTQAGEGTLSEALLQLQFDDEDLGALLGNSTDPAVFTDLASVDNSEFQQLLNQGIPVAPHTTEPMLMEYPEAITRLVTGAQRPPDPAPAPLGAPGLPNGLLSGDEDFSSIADMDFSALLSQISS

种属预测

种属预测:

score>80的预测可信度较高，可尝试用于WB检测。*预测模型主要基于免疫原序列比对，结果仅作参考，不作为质保凭据。

Species

Results

Score

Pig

100

Dog

100

Horse

Bovine

Sheep

Xenopus

Zebrafish

Chicken

Rabbit

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - Q04206 作为底物

Q04206

Site	PTM Type	Enzyme	Source
M1	Acetylation		Uniprot
K37	Methylation		Uniprot
K37	Sumoylation		Uniprot
C38	S-Nitrosylation		Uniprot
S42	Phosphorylation		Uniprot
S45	Phosphorylation		Uniprot
K56	Ubiquitination		Uniprot
K62	Ubiquitination		Uniprot
T71	Phosphorylation		Uniprot
S75	Phosphorylation		Uniprot
K79	Ubiquitination		Uniprot
K93	Ubiquitination		Uniprot
S112	Phosphorylation		Uniprot
K122	Acetylation		Uniprot
K122	Ubiquitination		Uniprot
K123	Acetylation		Uniprot
K123	Ubiquitination		Uniprot
S131	Phosphorylation		Uniprot
T136	Phosphorylation		Uniprot
R174	Methylation		Uniprot
S180	Phosphorylation		Uniprot
R187	Methylation		Uniprot
K195	Ubiquitination		Uniprot
S205	Phosphorylation		Uniprot
K218	Acetylation		Uniprot
K218	Methylation		Uniprot
K218	Ubiquitination		Uniprot
K221	Acetylation		Uniprot
K221	Methylation		Uniprot
S238	Phosphorylation		Uniprot
S240	Phosphorylation		Uniprot
T254	Phosphorylation		Uniprot
S261	Phosphorylation		Uniprot
S269	Phosphorylation		Uniprot
S276	Phosphorylation	P11309 (PIM1) , O94806 (PRKD3) , O75676 (RPS6KA4) , P17612 (PRKACA) , O75582 (RPS6KA5)	Uniprot
S281	Phosphorylation		Uniprot
T305	O-Glycosylation		Uniprot
T305	Phosphorylation		Uniprot
Y306	Phosphorylation		Uniprot
T308	Phosphorylation		Uniprot
K310	Acetylation		Uniprot
K310	Methylation		Uniprot
K310	Ubiquitination		Uniprot
S311	Phosphorylation	Q05513 (PRKCZ)	Uniprot
K314	Acetylation		Uniprot
K314	Methylation		Uniprot
K314	Ubiquitination		Uniprot
K315	Acetylation		Uniprot
K315	Methylation		Uniprot
K315	Ubiquitination		Uniprot
S316	Phosphorylation	P48729 (CSNK1A1)	Uniprot
S319	O-Glycosylation		Uniprot
T322	O-Glycosylation		Uniprot
S337	O-Glycosylation		Uniprot
S337	Phosphorylation		Uniprot
T352	O-Glycosylation		Uniprot
S374	O-Glycosylation		Uniprot
S374	Phosphorylation		Uniprot
S377	O-Glycosylation		Uniprot
T429	Phosphorylation		Uniprot
T435	Phosphorylation	P28482 (MAPK1)	Uniprot
S468	Phosphorylation	P49841 (GSK3B) , O14920 (IKBKB) , Q14164 (IKBKE)	Uniprot
S472	Phosphorylation		Uniprot
T505	Phosphorylation		Uniprot
S529	Phosphorylation	P68400 (CSNK2A1) , P47710 (CSN1S1)	Uniprot
S536	Phosphorylation	O15111 (CHUK) , O94806 (PRKD3) , Q9Y6K9 (IKBKG) , Q9UHD2 (TBK1) , Q9HCP0 (CSNK1G1) , Q16566 (CAMK4) , P51812 (RPS6KA3) , Q15418 (RPS6KA1) , Q00534 (CDK6) , O14920 (IKBKB) , P24723 (PRKCH) , Q14164 (IKBKE)	Uniprot
S543	Phosphorylation	P68400 (CSNK2A1)	Uniprot
S547	Phosphorylation	Q13315 (ATM)	Uniprot

研究背景

Q04206_TF65_HUMAN

功能:

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The heterodimeric RELA-NFKB1 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells. The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression.

翻译修饰:

Ubiquitinated by RNF182, leading to its proteasomal degradation. Degradation is required for termination of NF-kappa-B response.

Monomethylated at Lys-310 by SETD6. Monomethylation at Lys-310 is recognized by the ANK repeats of EHMT1 and promotes the formation of repressed chromatin at target genes, leading to down-regulation of NF-kappa-B transcription factor activity. Phosphorylation at Ser-311 disrupts the interaction with EHMT1 without preventing monomethylation at Lys-310 and relieves the repression of target genes (By similarity).

Phosphorylation at Ser-311 disrupts the interaction with EHMT1 and promotes transcription factor activity (By similarity). Phosphorylation on Ser-536 stimulates acetylation on Lys-310 and interaction with CBP; the phosphorylated and acetylated forms show enhanced transcriptional activity. Phosphorylation at Ser-276 by RPS6KA4 and RPS6KA5 promotes its transactivation and transcriptional activities.

Reversibly acetylated; the acetylation seems to be mediated by CBP, the deacetylation by HDAC3 and SIRT2. Acetylation at Lys-122 enhances DNA binding and impairs association with NFKBIA. Acetylation at Lys-310 is required for full transcriptional activity in the absence of effects on DNA binding and NFKBIA association. Acetylation at Lys-310 promotes interaction with BRD4. Acetylation can also lower DNA-binding and results in nuclear export. Interaction with BRMS1 promotes deacetylation of Lys-310. Lys-310 is deacetylated by SIRT2.

S-nitrosylation of Cys-38 inactivates the enzyme activity.

Sulfhydration at Cys-38 mediates the anti-apoptotic activity by promoting the interaction with RPS3 and activating the transcription factor activity.

Sumoylation by PIAS3 negatively regulates DNA-bound activated NF-kappa-B.

Proteolytically cleaved within a conserved N-terminus region required for base-specific contact with DNA in a CPEN1-mediated manner, and hence inhibits NF-kappa-B transcriptional activity.

细胞定位:

Nucleus. Cytoplasm.
Note: Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B) (PubMed:1493333). Colocalized with DDX1 in the nucleus upon TNF-alpha induction (PubMed:19058135). Colocalizes with GFI1 in the nucleus after LPS stimulation (PubMed:20547752). Translocation to the nucleus is impaired in L.monocytogenes infection (PubMed:20855622).

亚基结构:

Component of the NF-kappa-B p65-p50 complex. Component of the NF-kappa-B p65-c-Rel complex. Homodimer; component of the NF-kappa-B p65-p65 complex. Component of the NF-kappa-B p65-p52 complex. May interact with ETHE1. Binds TLE5 and TLE1. Interacts with TP53BP2. Binds to and is phosphorylated by the activated form of either RPS6KA4 or RPS6KA5. Interacts with ING4 and this interaction may be indirect. Interacts with CARM1, USP48 and UNC5CL. Interacts with IRAK1BP1 (By similarity). Interacts with NFKBID (By similarity). Interacts with NFKBIA. Interacts with GSK3B. Interacts with NFKBIB (By similarity). Interacts with NFKBIE. Interacts with NFKBIZ. Interacts with EHMT1 (via ANK repeats) (By similarity). Part of a 70-90 kDa complex at least consisting of CHUK, IKBKB, NFKBIA, RELA, ELP1 and MAP3K14. Interacts with HDAC3; HDAC3 mediates the deacetylation of RELA. Interacts with HDAC1; the interaction requires non-phosphorylated RELA. Interacts with CBP; the interaction requires phosphorylated RELA. Interacts (phosphorylated at 'Thr-254') with PIN1; the interaction inhibits p65 binding to NFKBIA. Interacts with SOCS1. Interacts with UXT. Interacts with MTDH and PHF11. Interacts with ARRB2. Interacts with NFKBIA (when phosphorylated), the interaction is direct; phosphorylated NFKBIA is part of a SCF(BTRC)-like complex lacking CUL1. Interacts with RNF25. Interacts (via C-terminus) with DDX1. Interacts with UFL1 and COMMD1. Interacts with BRMS1; this promotes deacetylation of 'Lys-310'. Interacts with NOTCH2 (By similarity). Directly interacts with MEN1; this interaction represses NFKB-mediated transactivation. Interacts with AKIP1, which promotes the phosphorylation and nuclear retention of RELA. Interacts (via the RHD) with GFI1; the interaction, after bacterial lipopolysaccharide (LPS) stimulation, inhibits the transcriptional activity by interfering with the DNA-binding activity to target gene promoter DNA. Interacts (when acetylated at Lys-310) with BRD4; leading to activation of the NF-kappa-B pathway. Interacts with MEFV. Interacts with CLOCK (By similarity). Interacts (via N-terminus) with CPEN1; this interaction induces proteolytic cleavage of p65/RELA subunit and inhibition of NF-kappa-B transcriptional activity. Interacts with FOXP3. Interacts with CDK5RAP3; stimulates the interaction of RELA with HDAC1, HDAC2 and HDAC3 thereby inhibiting NF-kappa-B transcriptional activity. Interacts with DHX9; this interaction is direct and activates NF-kappa-B-mediated transcription. Interacts with LRRC25. Interacts with TBX21 (By similarity). Interacts with KAT2A (By similarity). Interacts with ZBTB7A; involved in the control by RELA of the accessibility of target gene promoters. Directly interacts with DDX3X; this interaction may trap RELA in the cytoplasm, impairing nuclear relocalization upon TNF activating signals.

(Microbial infection) Interacts with human respiratory syncytial virus (HRSV) protein M2-1.

(Microbial infection) Interacts with molluscum contagiosum virus MC132.

(Microbial infection) Interacts with herpes virus 8 virus protein LANA1.

蛋白家族:

The transcriptional activation domain 3/TA3 does not participate to the direct transcriptional activity of RELA but is involved in the control by RELA of the accessibility of target gene promoters. Mediates interaction with ZBTB7A.

The transcriptional activation domain 1/TA1 and the transcriptional activation domain 2/TA2 have direct transcriptional activation properties (By similarity). The 9aaTAD motif found within the transcriptional activation domain 2 is a conserved motif present in a large number of transcription factors that is required for their transcriptional transactivation activity (PubMed:17467953).

研究领域

· Cellular Processes > Cell growth and death > Apoptosis. (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence. (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > cAMP signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway. (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway. (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Antifolate resistance.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Substance dependence > Cocaine addiction.

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer. (View pathway)

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Specific types > Pancreatic cancer. (View pathway)

· Human Diseases > Cancers: Specific types > Prostate cancer. (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia. (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia. (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer. (View pathway)

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Organismal Systems > Immune system > Chemokine signaling pathway. (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway. (View pathway)

· Organismal Systems > Development > Osteoclast differentiation. (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway. (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway. (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway. (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway. (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway. (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation. (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation. (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway. (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway. (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway. (View pathway)

· Organismal Systems > Endocrine system > Prolactin signaling pathway. (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

文献引用

1). Gut microbial metabolite trimethylamine N-oxide aggravates GVHD by inducing M1 macrophage polarization in mice. BLOOD, 2020 (PubMed: 32291445) [IF=20.3]

Application: IF/ICC Species: mouse Sample: BMDMs

Supplemental Figure 7.| TMAO induced NLRP3 expression by enhanced NF-κB nuclear localization. (A) Representative immunofluorescence staining of NF-κB (red: Alexa Fluor 594) in 300µM TMAO-treated BMDMs for 24h.Scale bar=25μm (B) Representative immunofluorescence image of p-NF-κB (red: Alexa Fluor 594) in BMDMs cultured with Triptolide (20nM), TMAO or TMAO+Triptolide for 24hrs. Scale bar=25μm.

2). An anti-inflammatory and neuroprotective biomimetic nanoplatform for repairing spinal cord injury. Bioactive Materials, 2022 (PubMed: 35845318) [IF=18.9]

Application: WB Species: Mice Sample: spinal cord

Fig. 2 Macrophage phenotype regulation based on RA@BSA@Cur NPs. (a) The schematic illustration of RA@BSA@Cur NPs regulated macrophage polarization under LPS. (b) The immunofluorescence and quantification results of RAW264.7 cultured different BSA-related NPs in LPS condition. CD86+ M1 macrophage (yellow arrow) and CD206+ M2 macrophage (white arrow), nuclei (DAPI: blue). Scale bar, 50 μm. (c&d) The flow cytometry analysis and quantification results of RAW264.7 (gated on F4/80+) cultured different BSA-related NPs in LPS condition. (e) The macrophages' M1 inhibition and M2 promotion regulated by RA@BSA@Cur NPs may be through the NF-κB pathway. (f) The inflammatory factors IL-6, TNF-α, and IL-4 changes after RA@BSA@Cur treatment. (n = 3 independent samples). Statistical differences were determined by using the Analysis of Variance (ANOVA) with Bonferroni's multiple comparison test (*p < 0.05, **p < 0.01, ***p < 0.001, ns: no significant; a.u. means arbitrary unit).

3). Tetrahedral Framework Nucleic Acids Based Small Interfering RNA Targeting Receptor for Advanced Glycation End Products for Diabetic Complications Treatment. ACS Nano, 2023 (PubMed: 37751401) [IF=17.1]

4). Gut dysbiosis promotes prostate cancer progression and docetaxel resistance via activating NF-κB-IL6-STAT3 axis. Microbiome, 2022 (PubMed: 35710492) [IF=15.5]

Application: WB Species: Mouse Sample: tumor tissue

Fig. 3 Intratumoral LPS activated NF-κB-IL6-STAT3 axis. A LPS levels in mouse feces and serum by ELISA; HE staining (scale bar, 50 μm) and histology score for colon tissue in the Abx and NC group. B Immunohistochemistry (scale bar, 50 μm) for LPS in subcutaneous and orthotopic tumor tissues and western blot of intratumoral LPS levels from three biological duplications for the Abx and NC group. C Transcription levels of cytokines by RT-qPCR and protein levels of IL6 in cell supernatant by ELISA in RM-1 cultured with LPS (100 μg/ml) for 24 h. D, E Immunofluorescence (scale bar, 100 μm) for p-p65 and p-STAT3 in RM-1 cultured with or without LPS for 24 h; western blot of relative proteins for RM-1 cultured with LPS at different concentrations for 24 h; transcription levels of IL6 by RT-qPCR and western blot of relative proteins in RM-1 cultured with LPS or LPS with BAY-11-7082 for 24 h; protein levels of p-STAT3 and STAT3 in RM-1 cultured with CM or CM with antibody-IL6 for 24 h. F, G IL6 levels in tumor tissue lysate and serum by ELISA. Western blot of relative proteins in tumor from three biological duplications. Immunohistochemistry of tumor tissues for p-p65- and p-STAT3-positive cell (scale bar, 50 μm). Statistical significance was assessed by unpaired Student’s T-test or LSD in one-way ANOVA. *p < 0.05, **p < 0.01, and ***p < 0.001: compared to the NC group; #p < 0.05, ##p < 0.01, and ###p < 0.001: compared to the LPS or CM group

Application: IF/ICC Species: Mouse Sample: tumor tissue

Application: IHC Species: Mouse Sample: tumor tissue

5). Opsonization Inveigles Macrophages Engulfing Carrier-Free Bilirubin/JPH203 Nanoparticles to Suppress Inflammation for Osteoarthritis Therapy. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024 (PubMed: 38593402) [IF=15.1]

6). OR11H1 Missense Variant Confers the Susceptibility to Vogt-Koyanagi-Harada Disease by Mediating Gadd45g Expression. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024 (PubMed: 38168905) [IF=15.1]

Application: WB Species: Human Sample: ARPE‐19 cells

Figure 3 OR11H1‐A63 increased GADD45G expression and activated the NF‐κB and MAPK pathways. ARPE‐19 cells were randomly divided into the OR11H1‐V63 + LPS and OR11H1‐A63 + LPS groups. After incubation with LPS (1 µg ml−1) for 24 h, cells were collected. A) Volcano plots of RNA‐seq assays. Black arrows represent GADD45G. B) Heatmaps of RNA‐seq assays. Red boxes represent GADD45G. C) Through RNA‐seq assays, the expression levels of PITX3, ABG1, CRB2, EBI3, CLECS5A, GADD45G, MYCT1, CD300LB, IRGM and GBP6 were measured by RT‒qPCR. D) The protein expression of GADD45G was measured by Western blotting. E) Peripheral blood of VKH patients was collected and RNA was extracted for qPCR experiment. The expression of GADD45G was measured by RT‒qPCR. (F) The protein expression of TLR4, MYD88, p‐p65, and p65 was detected by Western blotting. G) The protein expression of p‐p38, p38, p‐JNK, and JNK was measured by Western blotting. * P < 0.05, ** P < 0.01 by unpaired t test (n = 3).

7). CPAL, as a New Mediator of Cardiomyocyte Metabolic Alterations and Pyroptosis, Regulates Myocardial Infarction Injury in Mice. Engineering, 2023 [IF=12.8]

Application: WB Species: Mouse Sample:

Fig. 7. CPAL is an upstream regulator of NFκB. (a) Two specific regions (76–127 nt and 209–260 nt) of CPAL that were found to bind with NFκB using the online prediction website. (b) RIP analysis for CPAL-NFκB interaction. Immunoprecipitation of NFκB acquired a large amount of CPAL (**P < 0.01, compared with anti-IgG; n = 3). (c) Expression of P-NFκB and NFκB at the protein levels in each group (**P < 0.01, compared with sham group; ##P < 0.01, compared with +AAV9-sh-NC group; n = 4 to n = 6). (d) Immunohistochemical staining of P-NFκB protein in the infarct border zones of the left ventricular (**P < 0.01, compared with sham group; ##P < 0.01, compared with +AAV9-sh-NC group; n = 3 to n = 4). (e) Expression of P-NFκB and NFκB at the protein level in cardiomyocytes of control, LPS, +si-NC, and +si-CPAL groups (**P < 0.01, compared with control; #P < 0.05, compared with LPS group; n = 9). (f) Staining for P-NFκB (green) and α-actinin (red) proteins in the cardiomyocytes of control, LPS, +si-NC, and +si-CPAL groups (blue: DAPI; n = 4). (g) P-NFκB expression in the neonatal mouse cardiomyocytes of pcDNA3.1-OE-NC, pcDNA3.1-OE-CPAL, +ODNs-CPAL, and +ODNs-NC groups (**P < 0.01, compared with pcDNA3.1-OE-NC; ##P < 0.01, compared with pcDNA3.1-OE-CPAL; n = 5).

8). Mitochondrial STAT3 exacerbates LPS-induced sepsis by driving CPT1a-mediated fatty acid oxidation. Theranostics, 2022 (PubMed: 34976224) [IF=12.4]

Application: WB Species: Mice Sample: Lung tissues

Figure 8 Curcumin relieved LPS-induced sepsis. (A) After the last 4-OHT injection, Rosa26LSL-MLS-Stat3 and Rosa26LSL-MLS-Stat3;UbcERT2Cre/+ mice were injected with curcumin prior to LPS. Survival was monitored every 6 - 12 h after injection. The data shown represent a combination of two independent experiments. Statistical comparison of survival was performed with a log-rank test. **, P < 0.01, *, P < 0.05. (B) Serum samples were obtained from these mice and subjected to ELISA to examine MCP-5 levels. (C-D) The serum levels of LDH and albumin were assessed. (E) Lung tissues were removed, and the percentages of macrophages were analyzed by flow cytometry. (B-E) The data are representative of one of two independent experiments. Significance was calculated using a two-way ANOVA. **, P < 0.01, * P < 0.05, n.s., not significant. (F) Rosa26LSL-MLS-Stat3 and Rosa26LSL-MLS-Stat3;LyzCre/+ mice were injected with 10 mg/kg curcumin prior to LPS (20 mg/kg). Survival was monitored every 6 - 12 h after injection. Statistical comparison of survival was performed with a log-rank test. **, P < 0.01, *, P < 0.05. (G) BMDMs of the indicated genotypes were treated with 8 μM curcumin for 20 h and incubated with either 100 ng/mL LPS (30 min) or 100 ng/mL IFN-α (1 h) before harvesting. The cells were harvested, lysed, and subjected to a Western blot analysis. The membranes were blotted with the indicated antibodies. (H) Cells were treated with 8 μM curcumin for 20 h and incubated with 100 ng/mL LPS for another 15 min. Nuclei and cytoplasmic fractions were extracted. The levels of the indicated proteins were analyzed by a Western blot analysis. (I) BMDMs were treated with curcumin. After 20 h, these cells were stimulated with or without 100 ng/mL LPS for 6 h before loading. BMDMs were then treated sequentially with BSA-conjugated palmitate, oligomycin, FCCP, and ETO as indicated. The data are representative of one of two independent experiments performed with n = 5. (J) 4-OHT-treated BMDMs were treated with curcumin for 20 h, and then, the BMDMs were exposed to 100 ng/mL LPS and 10 μmol/L MG132 for an additional 6 h before harvesting. The cell lysates were isolated, IP with an anti-CPT1a antibody and analyzed by a Western blot analysis using an anti-ubiquitin antibody. (G, H and J) The results shown are representative of one of three independent experiments. (K) Schematic representation of the mitochondrial STAT3-mediated increase in FAO in a USP50-dependent manner in the LPS-induced sepsis model. Upon the LPS stimulation, mitochondrial STAT3 could induce CPT1a stabilization by promoting USP50 expression and facilitating CPT1a-USP50 binding, leading to a switch from glucose to an increased reliance on FAO for ATP production, which, in turn, further enhanced NF-κB nuclear localization, leading to a great amount of cytokine production.

9). Arsenic retention in erythrocytes and excessive erythrophagocytosis is related to low selenium status by impaired redox homeostasis. Redox Biology, 2022 (PubMed: 35500533) [IF=11.4]

Application: WB Species: Mice Sample: splenic macrophages

Fig. 6 Inflammation in splenic macrophages that phagocytosed As-exposed erythrocytes. (A–B) Relative mRNA levels of targets genes in macrophages that phagocytosed control erythrocytes or As-exposed erythrocytes were determined by qPCR (n = 3 per group) and data are presented. (C) Protein levels of targets in splenic macrophages phagocytosed control erythrocytes or As-exposed erythrocytes were analyzed by western blotting. (D) The levels of p-NFκB, iNOS and Cox-2 in mouse spleen sections were analyzed by immunohistochemistry. Differences between groups were analyzed by using the unpaired Student’s t tests. ***p < 0.001, **p < 0.005 or *p < 0.05 indicates significant difference.

Application: IHC Species: Mice Sample: splenic macrophages

10). Molecular mechanism of interleukin-17A regulating airway epithelial cell ferroptosis based on allergic asthma airway inflammation. Redox biology, 2023 (PubMed: 38035662) [IF=11.4]

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