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

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   规格 价格 库存
 50ul ¥1250 现货
 100ul ¥2300 现货
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货期: 当天发货

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, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
反应:
Human,Mouse,Rat,Monkey
预测:
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.
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:
基因/基因ID:
蛋白描述:
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.
蛋白序列:
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
91
Bovine
91
Sheep
91
Xenopus
0
Zebrafish
0
Chicken
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - Q04206 作为底物

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

研究背景

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).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
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). Huang S et al. Ras guanine nucleotide-releasing protein-4 promotes renal inflammatory injury in type 2 diabetes mellitus. Metabolism 2022 Feb 23;155177. (PubMed: 35218794) [IF=31.373]

2). Wu K et al. Gut microbial metabolite trimethylamine N-oxide aggravates GVHD by inducing M1 macrophage polarization in mice. Blood 2020 Apr 14 (PubMed: 32291445) [IF=25.476]

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.

3). Li R et al. Mitochondrial STAT3 exacerbates LPS-induced sepsis by driving CPT1a-mediated fatty acid oxidation. Theranostics 2022 Jan 1;12(2):976-998. (PubMed: 34976224) [IF=11.600]

4). Zhang Z et al. Clearance of apoptotic cells by mesenchymal stem cells contributes to immunosuppression via PGE2. EBioMedicine 2019 Jun 24 (PubMed: 31248835) [IF=11.205]

Application: WB    Species: mouse    Sample: MSCs

Fig. 5. |PGE2 Production in AC-MSCs is Dependent on NF-κB Signalling. (a) MSCs were cocultured with ACs at a ratio of 1:20 for the indicated time. The expressions of IκBα, p65 and their phosphorylated forms in MSCs were analysed by western blot.

5). Jia C et al. IL-37b alleviates endothelial cell apoptosis and inflammation in Kawasaki disease through IL-1R8 pathway. Cell Death Dis 2021 Jun 3;12(6):575. (PubMed: 34083516) [IF=9.685]

Application: WB    Species: Mouse    Sample: endothelial cells

Fig. 5 IL-37b inhibited the activation of ERK and NFκB in KD-treated ECs related to IL-1R8. a Effects of IL-37b treatment on the phosphorylation of ERK, JNK, p38, and NFκB p65 were assessed in the treated endothelial cells. b–e Quantitative analysis of these above proteins was conducted. Data are presented as mean ± SD (n = 3). Significance: *P < 0.05 vs. the HC group, and #P < 0.05 vs. the KD group. f, g Effects of IL-1R8 silencing on the activation of ERK and NFκB p65 were observed. Significance: *P < 0.05 vs. the HC group, #P < 0.05 vs. the KD group, and &P < 0.05 vs. the KD + IL-37b group. i The nuclear translocation of NFκB p65 was observed after silencing IL-1R8 expression (n = 3). Magnification: ×200, Scale bar = 100 μm. Experiments were done at least three times in triplicate.

6). Cai M et al. Herpes Simplex Virus 1 UL2 Inhibits the TNF-α–Mediated NF-κB Activity by Interacting With p65/p50. Front Immunol 2020 May 13;11:549. (PubMed: 32477319) [IF=8.786]

Application: WB    Species: Human    Sample: HEK293T cells

FIGURE 9 | p65 phosphorylation at Ser536 is suppressed by HSV-1 UL2. (A,C) HEK293T cells transfected with either HA empty vector or UL2-HA expression plasmid were stimulated with TNF-α (20 ng/mL) for the indicated times (0, 30, and 60 min) according to previous studies (59, 77), and then equal amounts of cell lysates were analyzed by WBs with phospho-NF-κB–p65 (Ser536) Ab (A), phospho-NF-κB–p65 (Ser276) Ab (C) (top panel), or anti-p65 pAb (second panel). Protein levels of UL2 (third panel) and β-actin (bottom panel) in the same cell lysates were also determined. (B,D) Densitometry of phospho-NF-κB–p65 Ser536 (B) and Ser276 bands (D) from (A,C), respectively, were normalized to loading control β-actin. Data were expressed as means ± SD from three independent experiments. ns, not significant and ***P < 0.001.

Application: WB    Species: human    Sample: HEK293T cells

FIGURE 9 | p65 phosphorylation at Ser536 is suppressed by HSV-1 UL2. (A,C) HEK293T cells transfected with either HA empty vector or UL2-HA expression plasmid were stimulated with TNF-α (20 ng/mL) for the indicated times (0, 30, and 60 min) according to previous studies (59, 77), and then equal amounts of cell lysates were analyzed by WBs with phospho-NF-κB–p65 (Ser536) Ab (A), phospho-NF-κB–p65 (Ser276) Ab (C) (top panel), or anti-p65 pAb (second panel). Protein levels of UL2 (third panel) and β-actin (bottom panel) in the same cell lysates were also determined. (B,D) Densitometry of phospho-NF-κB–p65 Ser536 (B) and Ser276 bands (D) from (A,C), respectively, were normalized to loading control β-actin.

7). Tao HC et al. CD47 Deficiency in Mice Exacerbates Chronic Fatty Diet-Induced Steatohepatitis Through Its Role in Regulating Hepatic Inflammation and Lipid Metabolism. Front Immunol 2020 Feb 25;11:148 (PubMed: 32158445) [IF=8.786]

Application: WB    Species: Mice    Sample: liver tissues

Figure 6 CD47 deficiency promotes HFD-induced nuclear factor-κB (NF-κB) activation and translocation. (A) Immunoblot analysis of phospho-NF-κB p65 (Ser536) protein in liver tissues from WT and CD47KO mice fed LFD or HFD (upper) and band density normalized to β-actin [lower; data are means (±SDs) of three independent experiments]. (B) Confocal images showing subcellular distribution of phosphorylated NF-κB (pNF-κB) (Ser536); pNF-κB (Ser536); and nucleus were stained in red by AF594 and in blue by DAPI, respectively. The representative images from four independent samples are shown. Scale bar represents 10 μm. Data are presented as mean ± SD. *p < 0.05 and ****P < 0.0001.

8). Liu X et al. Combination of resolvin E1 and lipoxin A4 promotes the resolution of pulpitis by inhibiting NF-κB activation through upregulating sirtuin 7 in dental pulp fibroblasts. Cell Prolif 2022 Apr 11;e13227. (PubMed: 35411569) [IF=8.755]

9). Ding R et al. Activating cGAS–STING axis contributes to neuroinflammation in CVST mouse model and induces inflammasome activation and microglia pyroptosis. J Neuroinflammation 2022 Jun 10;19(1):137. (PubMed: 35689216) [IF=8.322]

10). Yu Y et al. Cerium oxide nanozyme attenuates periodontal bone destruction by inhibiting ROS-NFκB pathway. Nanoscale 2022 Jan 28. (PubMed: 35088792) [IF=8.307]

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