Product: Phospho-p38 MAPK (Thr180/Tyr182) Antibody
Catalog: AF4001
Description: Rabbit polyclonal antibody to Phospho-p38 MAPK (Thr180/Tyr182)
Application: WB IHC IF/ICC IP
Cited expt.: WB, IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Xenopus
Mol.Wt.: 43 kDa; 41kD(Calculated).
Uniprot: Q16539
RRID: AB_2835330

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 100ul $350 In stock
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Product Info

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

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Xenopus(91%)
Clonality:
Polyclonal
Specificity:
Phospho-p38 MAPK (Thr180/Tyr182) Antibody detects endogenous levels of p38 MAPK only when phosphorylated at Thr180 and Tyr182 .
RRID:
AB_2835330
Cite Format: Affinity Biosciences Cat# AF4001, RRID:AB_2835330.
Conjugate:
Unconjugated.
Purification:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
Storage:
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.
Alias:

Fold/Unfold

CSAID Binding Protein 1; CSAID binding protein; CSAID-binding protein; Csaids binding protein; CSBP 1; CSBP 2; CSBP; CSBP1; CSBP2; CSPB1; Cytokine suppressive anti-inflammatory drug-binding protein; EXIP; MAP kinase 14; MAP kinase MXI2; MAP kinase p38 alpha; MAPK 14; MAPK14; MAX interacting protein 2; MAX-interacting protein 2; Mitogen Activated Protein Kinase 14; Mitogen activated protein kinase p38 alpha; Mitogen-activated protein kinase 14; Mitogen-activated protein kinase p38 alpha; MK14_HUMAN; Mxi 2; MXI2; p38 ALPHA; p38; p38 MAP kinase; p38 MAPK; p38 mitogen activated protein kinase; p38ALPHA; p38alpha Exip; PRKM14; PRKM15; RK; SAPK2A;

Immunogens

Immunogen:

A synthesized peptide derived from human p38 MAPK around the phosphorylation site of Thr180/Tyr182 .

Uniprot:
Gene(ID):
Expression:
Q16539 MK14_HUMAN:

Brain, heart, placenta, pancreas and skeletal muscle. Expressed to a lesser extent in lung, liver and kidney.

Description:
The protein encoded by this gene is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase is activated by various environmental stresses and proinflammatory cytokines.
Sequence:
MSQERPTFYRQELNKTIWEVPERYQNLSPVGSGAYGSVCAAFDTKTGLRVAVKKLSRPFQSIIHAKRTYRELRLLKHMKHENVIGLLDVFTPARSLEEFNDVYLVTHLMGADLNNIVKCQKLTDDHVQFLIYQILRGLKYIHSADIIHRDLKPSNLAVNEDCELKILDFGLARHTDDEMTGYVATRWYRAPEIMLNWMHYNQTVDIWSVGCIMAELLTGRTLFPGTDHIDQLKLILRLVGTPGAELLKKISSESARNYIQSLTQMPKMNFANVFIGANPLAVDLLEKMLVLDSDKRITAAQALAHAYFAQYHDPDDEPVADPYDQSFESRDLLIDEWKSLTYDEVISFVPPPLDQEEMES

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Rabbit
100
Xenopus
91
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

Function:

Serine/threonine kinase which acts as an essential component of the MAP kinase signal transduction pathway. MAPK14 is one of the four p38 MAPKs which play an important role in the cascades of cellular responses evoked by extracellular stimuli such as proinflammatory cytokines or physical stress leading to direct activation of transcription factors. Accordingly, p38 MAPKs phosphorylate a broad range of proteins and it has been estimated that they may have approximately 200 to 300 substrates each. Some of the targets are downstream kinases which are activated through phosphorylation and further phosphorylate additional targets. RPS6KA5/MSK1 and RPS6KA4/MSK2 can directly phosphorylate and activate transcription factors such as CREB1, ATF1, the NF-kappa-B isoform RELA/NFKB3, STAT1 and STAT3, but can also phosphorylate histone H3 and the nucleosomal protein HMGN1. RPS6KA5/MSK1 and RPS6KA4/MSK2 play important roles in the rapid induction of immediate-early genes in response to stress or mitogenic stimuli, either by inducing chromatin remodeling or by recruiting the transcription machinery. On the other hand, two other kinase targets, MAPKAPK2/MK2 and MAPKAPK3/MK3, participate in the control of gene expression mostly at the post-transcriptional level, by phosphorylating ZFP36 (tristetraprolin) and ELAVL1, and by regulating EEF2K, which is important for the elongation of mRNA during translation. MKNK1/MNK1 and MKNK2/MNK2, two other kinases activated by p38 MAPKs, regulate protein synthesis by phosphorylating the initiation factor EIF4E2. MAPK14 interacts also with casein kinase II, leading to its activation through autophosphorylation and further phosphorylation of TP53/p53. In the cytoplasm, the p38 MAPK pathway is an important regulator of protein turnover. For example, CFLAR is an inhibitor of TNF-induced apoptosis whose proteasome-mediated degradation is regulated by p38 MAPK phosphorylation. In a similar way, MAPK14 phosphorylates the ubiquitin ligase SIAH2, regulating its activity towards EGLN3. MAPK14 may also inhibit the lysosomal degradation pathway of autophagy by interfering with the intracellular trafficking of the transmembrane protein ATG9. Another function of MAPK14 is to regulate the endocytosis of membrane receptors by different mechanisms that impinge on the small GTPase RAB5A. In addition, clathrin-mediated EGFR internalization induced by inflammatory cytokines and UV irradiation depends on MAPK14-mediated phosphorylation of EGFR itself as well as of RAB5A effectors. Ectodomain shedding of transmembrane proteins is regulated by p38 MAPKs as well. In response to inflammatory stimuli, p38 MAPKs phosphorylate the membrane-associated metalloprotease ADAM17. Such phosphorylation is required for ADAM17-mediated ectodomain shedding of TGF-alpha family ligands, which results in the activation of EGFR signaling and cell proliferation. Another p38 MAPK substrate is FGFR1. FGFR1 can be translocated from the extracellular space into the cytosol and nucleus of target cells, and regulates processes such as rRNA synthesis and cell growth. FGFR1 translocation requires p38 MAPK activation. In the nucleus, many transcription factors are phosphorylated and activated by p38 MAPKs in response to different stimuli. Classical examples include ATF1, ATF2, ATF6, ELK1, PTPRH, DDIT3, TP53/p53 and MEF2C and MEF2A. The p38 MAPKs are emerging as important modulators of gene expression by regulating chromatin modifiers and remodelers. The promoters of several genes involved in the inflammatory response, such as IL6, IL8 and IL12B, display a p38 MAPK-dependent enrichment of histone H3 phosphorylation on 'Ser-10' (H3S10ph) in LPS-stimulated myeloid cells. This phosphorylation enhances the accessibility of the cryptic NF-kappa-B-binding sites marking promoters for increased NF-kappa-B recruitment. Phosphorylates CDC25B and CDC25C which is required for binding to 14-3-3 proteins and leads to initiation of a G2 delay after ultraviolet radiation. Phosphorylates TIAR following DNA damage, releasing TIAR from GADD45A mRNA and preventing mRNA degradation. The p38 MAPKs may also have kinase-independent roles, which are thought to be due to the binding to targets in the absence of phosphorylation. Protein O-Glc-N-acylation catalyzed by the OGT is regulated by MAPK14, and, although OGT does not seem to be phosphorylated by MAPK14, their interaction increases upon MAPK14 activation induced by glucose deprivation. This interaction may regulate OGT activity by recruiting it to specific targets such as neurofilament H, stimulating its O-Glc-N-acylation. Required in mid-fetal development for the growth of embryo-derived blood vessels in the labyrinth layer of the placenta. Also plays an essential role in developmental and stress-induced erythropoiesis, through regulation of EPO gene expression. Isoform MXI2 activation is stimulated by mitogens and oxidative stress and only poorly phosphorylates ELK1 and ATF2. Isoform EXIP may play a role in the early onset of apoptosis. Phosphorylates S100A9 at 'Thr-113'.

(Microbial infection) Activated by phosphorylation by M.tuberculosis EsxA in T-cells leading to inhibition of IFN-gamma production; phosphorylation is apparent within 15 minute and is inhibited by kinase-specific inhibitors SB203580 and siRNA.

PTMs:

Dually phosphorylated on Thr-180 and Tyr-182 by the MAP2Ks MAP2K3/MKK3, MAP2K4/MKK4 and MAP2K6/MKK6 in response to inflammatory citokines, environmental stress or growth factors, which activates the enzyme. Dual phosphorylation can also be mediated by TAB1-mediated autophosphorylation. TCR engagement in T-cells also leads to Tyr-323 phosphorylation by ZAP70. Dephosphorylated and inactivated by DUPS1, DUSP10 and DUSP16. PPM1D also mediates dephosphorylation and inactivation of MAPK14.

Acetylated at Lys-53 and Lys-152 by KAT2B and EP300. Acetylation at Lys-53 increases the affinity for ATP and enhances kinase activity. Lys-53 and Lys-152 are deacetylated by HDAC3.

Ubiquitinated. Ubiquitination leads to degradation by the proteasome pathway.

Subcellular Location:

Cytoplasm. Nucleus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Brain, heart, placenta, pancreas and skeletal muscle. Expressed to a lesser extent in lung, liver and kidney.

Family&Domains:

The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.

Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.

Research Fields

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

· Cellular Processes > Cellular community - eukaryotes > Signaling pathways regulating pluripotency of stem cells.   (View pathway)

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

· Environmental Information Processing > Signal transduction > Rap1 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 > TNF signaling pathway.   (View pathway)

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

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

· 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 > Leishmaniasis.

· 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 > Influenza A.

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

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Organismal Systems > Circulatory system > Adrenergic signaling in cardiomyocytes.   (View pathway)

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

· Organismal Systems > Immune system > Platelet activation.   (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 > Immune system > Leukocyte transendothelial migration.   (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 > Progesterone-mediated oocyte maturation.

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

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). 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:

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).

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

3). Cyanidin-3-O-glucoside restores spermatogenic dysfunction in cadmium-exposed pubertal mice via histone ubiquitination and mitigating oxidative damage. JOURNAL OF HAZARDOUS MATERIALS, 2020 (PubMed: 31796358) [IF=12.2]

Application: WB    Species: Mice    Sample: testis

Figure 8 The representative photographs and grayscale analysis of proteins in testis from mice treated for 30 days involved in MAPK signaling pathway. (A) JNK and p-JNK. (B) ERK and p-ERK. (C) p38 and p-p38. Comparison between all groups was evaluated through One-way ANOVA. Mean±SD. n=4. **p<0.01, *p<0.05, compared with control group. ##p<0.01, #p<0.05, compared with Cd group. ns, not significant.

4). Ly6G+ Neutrophils and Interleukin-17 Are Essential in Protection against Rodent Malaria Caused by Plasmodium berghei ANKA. Research, 2024 [IF=11.0]

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). Salidroside attenuates HALI via IL-17A-mediated ferroptosis of alveolar epithelial cells by regulating Act1-TRAF6-p38 MAPK pathway. Cell Communication and Signaling, 2022 (PubMed: 36411467) [IF=8.4]

8). MLKL signaling regulates macrophage polarization in acute pancreatitis through CXCL10. Cell death & disease, 2023 (PubMed: 36828808) [IF=8.1]

9). LncRNA CD27-AS1 promotes acute myeloid leukemia progression through the miR-224-5p/PBX3 signaling circuit. Cell Death & Disease, 2021 (PubMed: 34006845) [IF=8.1]

Application: WB    Species: Human    Sample: AML cells

Fig. 5 CD27-AS1 regulates MAPK signaling pathway in the AML cell lines. a HL-60 and KG-1 cells were infected with LV-CD27-AS1 and LV-CD27- AS1-Sh1. Protein levels of P38, p-P38, JNK, p-JNK, p-C-raf, p-MEK1/2, ERK, and p-ERK were detected using western blotting. b Densitometry analysis of protein levels in both cells was performed. c U0126, a MEK1/2 inhibitor, was used to treat the AML cells with CD27-AS1 upregulation. Relative protein levels of p-ERK and ERK were measured using western blotting. d CCK-8 assay was performed to check cell viability. N = 3. Data were shown as means ± SD. *P < 0.05, **P < 0.01, and ***P < 0.001.

10). Cetuximab promotes RSL3-induced ferroptosis by suppressing the Nrf2/HO-1 signalling pathway in KRAS mutant colorectal cancer. Cell Death & Disease, 2021 (PubMed: 34775496) [IF=8.1]

Application: WB    Species: Human    Sample: HCT116 and DLD-1 cells

Fig. 4 Cetuximab activates p38 MAPK and regulates the Nrf2/HO-1 axis. A Western blot analysis of p-p38, total p38, Nrf2 and HO-1 expression levels in HCT116 and DLD-1 cells incubated with cetuximab (100 μg/ml), SB202190 (1 μM) or cetuximab in combination with SB202190 for 24 h. B HCT116 and DLD-1 cells were treated with cetuximab (100 μg/ml) or RSL3 (1 μM) in the absence or presence of SB202190 (1 μM) for 24 h, and cell viability was assessed by the CCK-8 assay. C The protein levels of Nrf2 and HO-1 in HCT116 and DLD-1 cells or Nrf2 overexpressed HCT116 and DLD-1 cells treated with RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. D HCT116 and DLD-1 cells with overexpression Nrf2 were treated with or without RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. Cell viability was assessed by CCK-8 assays. E The protein level of HO-1 in HCT116 and DLD-1 cells or HO-1 overexpressed HCT116 and DLD-1 cells treated with RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. F HCT116 and DLD-1 cells with overexpression HO-1 were treated with or without RSL3 (1 μM) combination with cetuximab (100 μg/ml) for 24 h. Cell viability was assessed by CCK-8 assays. G–H HCT116 and DLD-1 cells were treated with cetuximab (100 μg/ml) or RSL3 (1 μM) with or without t-BHQ (20 μM) or hemin (20 μM) for 24 h, and cell viability was assessed by the CCK-8 assay. **P < 0.01.

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