产品: 磷酸化 JNK1/2/3 (Thr183+Tyr185) 抗体
货号: AF3318
描述: Rabbit polyclonal antibody to Phospho-JNK1/2/3 (Thr183+Tyr185)
应用: WB IHC IF/ICC
文献验证: WB, IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
蛋白号: P45983 | P45984 | P53779
RRID: AB_2834737

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:100-1:500, IF/ICC 1:100-1:500
*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:
Phospho-JNK1/2/3 (Thr183+Tyr185) Antibody detects endogenous levels of JNK1/2/3 only when phosphorylated at Threonine 183+Tyrosine 185.
RRID:
AB_2834737
引用格式: Affinity Biosciences Cat# AF3318, RRID:AB_2834737.
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, 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

C Jun kinase 2; c Jun N terminal kinase 1; c Jun N terminal kinase 2; c Jun N terminal kinase 3; c-Jun N-terminal kinase 1; JNK 46; JNK 55; JNK; JNK-46; JNK1; JNK1A2; JNK2; JNK21B1/2; JNK2A; JNK2ALPHA; JNK2B; JNK2BETA; JNK3 alpha protein kinase; JNK3; JNK3A; Jun kinase; JUN N terminal kinase; MAP kinase 10; MAP kinase 8; MAP kinase 9; MAP kinase p49 3F12; MAPK 10; MAPK 8; MAPK 9; MAPK10; mapk8; MAPK9; Mitogen activated protein kinase 10; Mitogen activated protein kinase 8; Mitogen activated protein kinase 8 isoform JNK1 alpha1; Mitogen activated protein kinase 8 isoform JNK1 beta2; Mitogen activated protein kinase 9; Mitogen-activated protein kinase 8; MK08_HUMAN; p493F12; p54a; p54aSAPK; p54bSAPK; PRKM10; PRKM8; PRKM9; SAPK; SAPK(beta); SAPK1; SAPK1a; SAPK1b; SAPK1c; Stress activated protein kinase 1; Stress activated protein kinase 1a; Stress activated protein kinase 1b; Stress activated protein kinase 1c; Stress activated protein kinase beta; Stress activated protein kinase JNK1; Stress activated protein kinase JNK2; Stress activated protein kinase JNK3; Stress-activated protein kinase 1c; Stress-activated protein kinase JNK1; c Jun kinase 2; C Jun N terminal kinase 2; c-Jun N-terminal kinase 2; JNK 55; JNK-55; JNK2 alpha; JNK2; JNK2 beta; JNK2A; JNK2alpha; JNK2B; JNK2BETA; Jun kinase; MAP kinase 9; MAPK 9; Mapk9; Mitogen activated protein kinase 9; Mitogen-activated protein kinase 9; MK09_HUMAN; P54a; p54aSAPK; PRKM9; Protein kinase, mitogen-activated, 9; SAPK alpha; SAPK; SAPK1a; Stress activated protein kinase 1a; Stress-activated protein kinase JNK2; c Jun kinase 3; c-Jun N-terminal kinase 3; cJun N terminal kinase 3; FLJ12099; FLJ33785; JNK3 alpha protein kinase; JNK3; JNK3A; MAP kinase 10; MAP kinase; MAP kinase p49 3F12; MAPK 10; Mapk10; MGC50974; mitogen activated protein kinase 10; Mitogen-activated protein kinase 10; MK10_HUMAN; p493F12; p54bSAPK; PRKM10; protein kinase mitogen activated 10; SAPK1b; Stress activated protein kinase 1b; stress activated protein kinase beta; Stress activated protein kinase JNK3; Stress-activated protein kinase JNK3;

抗原和靶标

免疫原:

A synthesized peptide derived from human JNK1/2/3 around the phosphorylation site of Thr183+Tyr185.

基因/基因ID:
描述:
JNK3 a protein kinase of the MAPK family that is potently activated by a variety of environmental stress and pro-inflammatory cytokines. Brain-selective JNK isoform.

研究领域

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

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

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

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

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Tight junction.   (View pathway)

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

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

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

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

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

· Genetic Information Processing > Folding, sorting and degradation > Protein processing in endoplasmic reticulum.   (View pathway)

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

· Human Diseases > Endocrine and metabolic diseases > Type II diabetes mellitus.

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

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

· 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: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· 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 > Influenza A.

· 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: Specific types > Colorectal cancer.   (View pathway)

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

· Human Diseases > Cancers: Overview > Choline metabolism in cancer.   (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 > 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 > Fc epsilon RI signaling pathway.   (View pathway)

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

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

· Organismal Systems > Nervous system > Dopaminergic synapse.

· Organismal Systems > Sensory system > Inflammatory mediator regulation of TRP channels.   (View pathway)

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

· Organismal Systems > Endocrine system > Progesterone-mediated oocyte maturation.

· 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). SARS-CoV-2 envelope protein impairs airway epithelial barrier function and exacerbates airway inflammation via increased intracellular Cl- concentration. Signal transduction and targeted therapy, 2024 (PubMed: 38528022) [IF=40.8]

Application: WB    Species: Human    Sample:

Fig. 7 SARS-CoV-2 envelope (E) protein down-regulated tight junction proteins and triggered inflammation and intracellular Cl− accumulation in human primary cultured airway epithelial cells (hPAECs). a Representative immunoblots showing the expression level of ZO-1, occludin and claudin-4 in hPAECs stimulated with E protein (50 μg/ml) for 6 h. GAPDH served as a loading control. b Immunofluorescence images showing the expression of ZO-1 in hPAECs, in the absence or presence of E protein stimulation for 6 h. c Quantitative real-time PCR analyses showing the expression of pro-inflammatory cytokines in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 3). d Representative immunoblots showing the expression of cystic fibrosis transmembrane conductance regulator (CFTR) and the phosphorylation level of JNK, serum/glucocorticoid regulated kinase 1 (SGK1) and IκB in hPAECs after stimulation with the E protein (50 μg/ml) for 12 h. GAPDH served as a loading control. e Immunofluorescence images showing the phosphorylation of JNK in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. f Immunofluorescence images showing the phosphorylation of SGK1 in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. g Quantitative real-time PCR analyses showing the expression of phosphodiesterase 4 (PDE4) in hPAECs stimulated with E protein (50 μg/ml) for the indicated different time points (n = 3). h Intracellular Cl− concentration ([Cl−]i) was measured in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 25 cells for each group). Data are shown as means ± S.D. **P 

Application: IF/ICC    Species: Human    Sample: BEAS-2B cells

Fig. 7 SARS-CoV-2 envelope (E) protein down-regulated tight junction proteins and triggered inflammation and intracellular Cl− accumulation in human primary cultured airway epithelial cells (hPAECs). a Representative immunoblots showing the expression level of ZO-1, occludin and claudin-4 in hPAECs stimulated with E protein (50 μg/ml) for 6 h. GAPDH served as a loading control. b Immunofluorescence images showing the expression of ZO-1 in hPAECs, in the absence or presence of E protein stimulation for 6 h. c Quantitative real-time PCR analyses showing the expression of pro-inflammatory cytokines in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 3). d Representative immunoblots showing the expression of cystic fibrosis transmembrane conductance regulator (CFTR) and the phosphorylation level of JNK, serum/glucocorticoid regulated kinase 1 (SGK1) and IκB in hPAECs after stimulation with the E protein (50 μg/ml) for 12 h. GAPDH served as a loading control. e Immunofluorescence images showing the phosphorylation of JNK in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. f Immunofluorescence images showing the phosphorylation of SGK1 in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. g Quantitative real-time PCR analyses showing the expression of phosphodiesterase 4 (PDE4) in hPAECs stimulated with E protein (50 μg/ml) for the indicated different time points (n = 3). h Intracellular Cl− concentration ([Cl−]i) was measured in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 25 cells for each group). Data are shown as means ± S.D. **P 

2). Hepatoma cell-intrinsic TLR9 activation induces immune escape through PD-L1 upregulation in hepatocellular carcinoma. Theranostics, 2023 (PubMed: 32483468) [IF=12.4]

3). Mucin 17 inhibits the progression of human gastric cancer by limiting inflammatory responses through a MYH9-p53-RhoA regulatory feedback loop. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, 2019 (PubMed: 31262330) [IF=11.3]

Application: WB    Species: human    Sample: AGS cells

Fig. 5| MUC17 protects GC cells against inflammatory stimulation by regulating the p38 pathway. a MUC17 regulated the expression of pJNK,pERK, and pp38 MAPK in MUC17 knocked-down AGS cells (left) and truncated MUC17 overexpressed MKN45 cells (right).

4). Elamipretide alleviates pyroptosis in traumatically injured spinal cord by inhibiting cPLA2-induced lysosomal membrane permeabilization. Journal of Neuroinflammation, 2023 (PubMed: 36609266) [IF=9.3]

5). The microRNA-211-5p/P2RX7/ERK/GPX4 axis regulates epilepsy-associated neuronal ferroptosis and oxidative stress. Journal of neuroinflammation, 2024 (PubMed: 38191407) [IF=9.3]

6). LAGE3 promoted cell proliferation, migration, and invasion and inhibited cell apoptosis of hepatocellular carcinoma by facilitating the JNK and ERK signaling pathway. CELLULAR & MOLECULAR BIOLOGY LETTERS, 2021 (PubMed: 34837962) [IF=9.2]

Application: WB    Species: Human    Sample: Hep-3B cells

Fig. 6 LAGE3 aggravated HCC progression by enhancing the JNK and ERK signaling pathway. Hep-3B cells were transfected with LAGE3-OE and then incubated with ERK inhibitor SCH772984 or JNK inhibitor SP600125. A Western blot bands of p-p38, p38, p-JNK, JNK, p-ERK, and ERK in Hep3B cells. B Proliferation ability of Hep3B cells. C–D Migration and invasion abilities of Hep3B cells. Data are shown as mean ± standard deviation. *p < 0.05, **p < 0.01

7). c-FLIP Protects Cardiac Microcirculation in Sepsis-Induced Myocardial Dysfunction Via FUNDC1-Mediated Regulation of Mitochondrial Autophagy. JACC. Basic to translational science, 2025 (PubMed: 40372306) [IF=8.4]

8). Melatonin restores endoplasmic reticulum homeostasis to protect injured neurons in a rat model of chronic cervical cord compression. JOURNAL OF PINEAL RESEARCH, 2023 (PubMed: 36732085) [IF=8.3]

9). N6-methyladenosine Reader IGF2BP2-modified HMMR Promotes Non-small Cell Lung Cancer Metastasis via Interaction with MAP4K4. International journal of biological sciences, 2025 (PubMed: 39990663) [IF=8.2]

10). IL-37b alleviates endothelial cell apoptosis and inflammation in Kawasaki disease through IL-1R8 pathway. Cell Death & Disease, 2021 (PubMed: 34083516) [IF=8.1]

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.

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