产品: RIP3 抗体
货号: AF7942
描述: Rabbit polyclonal antibody to RIP3
应用: WB IHC
反应: Human, Mouse, Rat
分子量: 57kDa.; 53kD(Calculated).
蛋白号: Q9QZL0
RRID: AB_2844305

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200
*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,Mouse,Rat
克隆:
Polyclonal
特异性:
RIP3 Antibody detects endogenous levels of total RIP3.
RRID:
AB_2844305
引用格式: Affinity Biosciences Cat# AF7942, RRID:AB_2844305.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

Receptor interacting protein 3; Receptor interacting serine threonine kinase 3; Receptor interacting serine/threonine protein kinase 3; Receptor-interacting protein 3; Receptor-interacting serine/threonine-protein kinase 3; RIP 3; RIP like protein kinase 3; RIP-3; RIP-like protein kinase 3; RIPK 3; RIPK3; RIPK3_HUMAN;

抗原和靶标

免疫原:

A synthesized peptide derived from mouse RIP3, corresponding to a region within the internal amino acids.

Uniprot:
表达:
Q9QZL0 RIPK3_MOUSE:

Expressed in embryo and in adult spleen, liver, testis, heart, brain and lung.

序列:
MSSVKLWPTGASAVPLVSREELKKLEFVGKGGFGVVFRAHHRTWNHDVAVKIVNSKKISWEVKAMVNLRNENVLLLLGVTEDLQWDFVSGQALVTRFMENGSLAGLLQPECPRPWPLLCRLLQEVVLGMCYLHSLNPPLLHRDLKPSNILLDPELHAKLADFGLSTFQGGSQSGSGSGSGSRDSGGTLAYLDPELLFDVNLKASKASDVYSFGILVWAVLAGREAELVDKTSLIRETVCDRQSRPPLTELPPGSPETPGLEKLKELMIHCWGSQSENRPSFQDCEPKTNEVYNLVKDKVDAAVSEVKHYLSQHRSSGRNLSAREPSQRGTEMDCPRETMVSKMLDRLHLEEPSGPVPGKCPERQAQDTSVGPATPARTSSDPVAGTPQIPHTLPFRGTTPGPVFTETPGPHPQRNQGDGRHGTPWYPWTPPNPMTGPPALVFNNCSEVQIGNYNSLVAPPRTTASSSAKYDQAQFGRGRGWQPFHK

翻译修饰 - Q9QZL0 作为底物

Site PTM Type Enzyme
S2 Phosphorylation
K5 Ubiquitination
S165 Phosphorylation
S184 Phosphorylation
T231 Phosphorylation
S232 Phosphorylation Q9QZL0 (Ripk3)
T257 Phosphorylation
K264 Ubiquitination
S304 Phosphorylation
S326 Phosphorylation
T338 Phosphorylation
S353 Phosphorylation
S369 Phosphorylation
T374 Phosphorylation
S380 Phosphorylation
T392 Phosphorylation
T399 Phosphorylation P63085 (Mapk1)
R477 Methylation
R479 Methylation

翻译修饰 - Q9QZL0 作为激酶

Substrate Site Source
Q6PHZ2 (Camk2d) T287 Uniprot
Q9D2Y4 (Mlkl) S345 Uniprot
Q9D2Y4 (Mlkl) S347 Uniprot
Q9D2Y4 (Mlkl) T349 Uniprot
Q9QZL0 (Ripk3) S232 Uniprot

研究背景

功能:

Serine/threonine-protein kinase that activates necroptosis and apoptosis, two parallel forms of cell death. Necroptosis, a programmed cell death process in response to death-inducing TNF-alpha family members, is triggered by RIPK3 following activation by ZBP1. Activated RIPK3 forms a necrosis-inducing complex and mediates phosphorylation of MLKL, promoting MLKL localization to the plasma membrane and execution of programmed necrosis characterized by calcium influx and plasma membrane damage. In addition to TNF-induced necroptosis, necroptosis can also take place in the nucleus in response to orthomyxoviruses infection: following ZBP1 activation, which senses double-stranded Z-RNA structures, nuclear RIPK3 catalyzes phosphorylation and activation of MLKL, promoting disruption of the nuclear envelope and leakage of cellular DNA into the cytosol. Also regulates apoptosis: apoptosis depends on RIPK1, FADD and CASP8, and is independent of MLKL and RIPK3 kinase activity. Phosphorylates RIPK1: RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation (By similarity). In some cell types, also able to restrict viral replication by promoting cell death-independent responses. In response to flavivirus infection in neurons, promotes a cell death-independent pathway that restricts viral replication: together with ZBP1, promotes a death-independent transcriptional program that modifies the cellular metabolism via up-regulation expression of the enzyme ACOD1/IRG1 and production of the metabolite itaconate. Itaconate inhibits the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes. RIPK3 binds to and enhances the activity of three metabolic enzymes: GLUL, GLUD1, and PYGL (By similarity). These metabolic enzymes may eventually stimulate the tricarboxylic acid cycle and oxidative phosphorylation, which could result in enhanced ROS production (By similarity).

翻译修饰:

RIPK1 and RIPK3 undergo reciprocal auto- and trans-phosphorylation (By similarity). Autophosphorylated following interaction with ZBP1. Phosphorylation of Ser-204 plays a role in the necroptotic function of RIPK3 (By similarity). Autophosphorylates at Thr-231 and Ser-232 following activation by ZBP1: phosphorylation at these sites is a hallmark of necroptosis and is required for binding MLKL. Phosphorylation at Thr-187 is important for its kinase activity, interaction with PELI1 and for its ability to mediate TNF-induced necroptosis (By similarity).

Polyubiquitinated with 'Lys-48' and 'Lys-63'-linked chains by BIRC2/c-IAP1 and BIRC3/c-IAP2, leading to activation of NF-kappa-B. Ubiquitinated by STUB1 leading to its subsequent proteasome-dependent degradation.

细胞定位:

Cytoplasm>Cytosol. Nucleus.
Note: Mainly cytoplasmic (PubMed:32200799, PubMed:32296175). Present in the nucleus in response to influenza A virus (IAV) infection (PubMed:32200799).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
组织特异性:

Expressed in embryo and in adult spleen, liver, testis, heart, brain and lung.

亚基结构:

Interacts (via RIP homotypic interaction motif) with RIPK1 (via RIP homotypic interaction motif); this interaction induces RIPK1 phosphorylation and formation of a RIPK1-RIPK3 necrosis-inducing complex. Interacts with MLKL; the interaction is direct and triggers necroptosis. Interacts with ZBP1 (via RIP homotypic interaction motif); interaction with ZBP1 activates RIPK3, triggering necroptosis. Upon TNF-induced necrosis, the RIPK1-RIPK3 dimer further interacts with PGAM5 and MLKL; the formation of this complex leads to PGAM5 phosphorylation and increase in PGAM5 phosphatase activity (By similarity). Binds TRAF2 and is recruited to the TNFR-1 signaling complex (By similarity). Interacts with PYGL, GLUL and GLUD1; these interactions result in activation of these metabolic enzymes (By similarity). Interacts with BIRC2/c-IAP1, BIRC3/c-IAP2 and XIAP/BIRC4 (By similarity). Interacts with ARHGEF2 (By similarity). Interacts with PELI1 (via atypical FHA domain); the phosphorylated form at Thr-187 binds preferentially to PELI1. Interacts with BUB1B, TRAF2 and STUB1 (By similarity). Interacts with CASP6 (By similarity).

(Microbial infection) Interacts (via RIP homotypic interaction motif) with murid herpesvirus protein RIR1; this interaction disrupts RIP3-RIP1 interactions characteristic of TNF-alpha induced necroptosis, thereby suppressing this death pathway.

蛋白家族:

The RIP homotypic interaction motif (RHIM) mediates interaction with the RHIM motif of RIPK1. Both motifs form a hetero-amyloid serpentine fold, stabilized by hydrophobic packing and featuring an unusual Cys-Ser ladder of alternating Ser (from RIPK1) and Cys (from RIPK3).

Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family.

文献引用

1). 1, 3-Dichloro-2-propanol-Induced Renal Tubular Cell Necroptosis through the ROS/RIPK3/MLKL Pathway. Journal of Agricultural and Food Chemistry, 2022 (PubMed: 36000575) [IF=6.1]

2). Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel. Frontiers in Cell and Developmental Biology, 2021 (PubMed: 34778271) [IF=5.5]

3). Tanshinone I exerts cardiovascular protective effects in vivo and in vitro through inhibiting necroptosis via Akt/Nrf2 signaling pathway. Chinese Medicine, 2021 (PubMed: 34183021) [IF=4.9]

Application: WB    Species: Rat    Sample: H9c2 cells

Fig. 2 TI ameliorated t‑BHP induced cell necroptosis via RIP1/RIP3/MLKL pathway. a H9c2 cells were cultured with Nec-1 for 12 h. b Cells were exposed to t-BHP (150 μM) for 10 h after treated with Nec-1 for 2 h. c Cells were exposed to t-BHP (150 μM) for 10 h after treated with TI (1 μM) or Nec-1 (100 μM) for 2 h. MTT was employed to detect cell viability. d Cells were treated with t-BHP (150 μM) for 10 h when pretreated with TI (1 μM) or Nec-1 (100 μM) for 2 h, the LDH level was monitored by LDH kit. e–h Pretreated with TI (0.25, 0.5, and 1 μM) or Nec-1 (100 μM) for 2 h respectively, then exposed to t-BHP (150 μM) for 4 h, the protein expression was determined by western blotting. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001 vs. t-BHP group

4). 3-Monochloropropane-1,2-diol esters induce HepG2 cells necroptosis via CTSB/TFAM/ROS pathway. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2024 (PubMed: 38408632) [IF=4.3]

5). Alcohol induces hepatocytes necroptosis through the LC3/RIPK1/RIPK3 pathway. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2023 (PubMed: 37898230) [IF=4.3]

6). Excessive intragastric alcohol administration exacerbates hepatic encephalopathy and provokes neuronal cell death in male rats with chronic liver disease. Journal of neuroscience research, 2024 (PubMed: 38680084) [IF=4.2]

Application: WB    Species: Rat    Sample:

FIGURE 4 Neuronal loss, oxidative stress, apoptosis, and necroptosis. Protein expression levels of NeuN, SMI311, and GFAP remained unchanged in (a) frontal cortex and decreased significantly in (b) cerebellum of BDL-alcohol rats (*p 

7). Sugarcane leaf polysaccharide exerts a therapeutic effect on cardiovascular diseases through necroptosis. Heliyon, 2023 (PubMed: 38027563) [IF=4.0]

Application: WB    Species: Rat    Sample: H9c2 cells

Fig. 5 SLP alleviated TBHP-stimulated cell necroptosis through the RIP1/RIP3/MLKL signaling pathway in H9c2 cells. (A) H9c2 cells were incubated with SLP (25, 50, and 100 μg/mL) and then treated with TBHP (100 μM). The protein expression of p-RIP1, RIP1, p-RIP3, RIP3, p-MLKL, and MLKL was determined using western blotting. (B–D) Statistical analysis of the above protein expressions. n = 3. ##p < 0.01, ###p < 0.001, vs. the control group. *p < 0.05, **p < 0.01, ***p < 0.001, vs. TBHP group.

8). Itaconate inhibits corticosterone-induced necroptosis and neuroinflammation via up-regulating menin in HT22 cells. Journal of physiology and biochemistry, 2024 (PubMed: 38427168) [IF=3.4]

9). Metformin attenuates lung ischemia-reperfusion injury and necroptosis through AMPK pathway in type 2 diabetic recipient rats. BMC pulmonary medicine, 2024 (PubMed: 38745191) [IF=3.1]

Application: WB    Species: Rat    Sample:

Fig. 7 Metformin inhibited the necroptosis in type 2 diabetic lung transplant recipient rats. (A) RIPK1 representative western blot image. Full-length blots/gels are presented in Supplementary Fig. 2. (B) RIPK1 expression levels in lung grafts (n = 3). (C) RIPK3 representative western blot image. Full-length blots/gels are presented in Supplementary Fig. 3. (D) RIPK3 expression levels in lung grafts (n = 3). (E) MLKL representative western blot image. Full-length blots/gels are presented in Supplementary Fig. 4. (F) MLKL expression levels in lung grafts (n = 3). Compared with CS group, *P

10). Regulation of endoplasmic reticulum stress on autophagy and apoptosis of nucleus pulposus cells in intervertebral disc degeneration and its related mechanisms. PeerJ, 2024 (PubMed: 38666076) [IF=2.7]

Application: WB    Species: Human    Sample:

Figure 6 ERS affects the occurrence and development of IVDD by regulating programmed death. (A) ELISA detected the levels of IL-1β, TNF-α, iNOS and IL-6. (B) Western blot was used to detect the expressions of RIP1 and RIP3. The quantitative values are expressed as mean ± SD from at least three independent experiments

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