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anti-Human MAPK12 Antibodies:
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Human Polyclonal MAPK12 Primary Antibody for IHC (fro), ELISA - ABIN543864
Knebel, Morrice, Cohen: A novel method to identify protein kinase substrates: eEF2 kinase is phosphorylated and inhibited by SAPK4/p38delta. in The EMBO journal 2001
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Human Polyclonal MAPK12 Primary Antibody for IHC (p), ELISA - ABIN543748
Julien, Coulombe, Meloche: Nuclear export of ERK3 by a CRM1-dependent mechanism regulates its inhibitory action on cell cycle progression. in The Journal of biological chemistry 2003
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Cow (Bovine) Polyclonal MAPK12 Primary Antibody for WB - ABIN611036
Fulda, Meyer, Debatin: Inhibition of TRAIL-induced apoptosis by Bcl-2 overexpression. in Oncogene 2002
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Human Polyclonal MAPK12 Primary Antibody for PLA, WB - ABIN520005
Liu, Chen, Chau, Jan, Chen, Hsu, Lin, Juang, Lu, Cheng, Chen, Chang, Ting, Kao, Hsiao, Huang: Analysis of protein-protein interactions in cross-talk pathways reveals CRKL protein as a novel prognostic marker in hepatocellular carcinoma. in Molecular & cellular proteomics : MCP 2013
Study propose a model for sequential roles of MPK12, HT1, and GHR1 in the ABA-independent regulation of SLAC1 during CO2-induced stomatal closure.
MPK9 and MPK12 are positive regulators of salicylic acid signaling in Arabidopsis guard cells.
MPK9 and MPK12 are key regulators mediating both abscisic acid (ABA) and Methyl jasmonate (MeJA) signalling in guard cells.
MPK9 and MPK12 function redundantly downstream of extracellular reactive oxygen production and intracellular accumulation, cytosolic alkalisation and Ca(2+)cytosolic oscillation in yeast elcictor-induced stomatal closure
MPK9 and MPK12 act downstream of ROS and cytosolic Ca2+ and upstream of anion channels in the guard cell abscisic acid signaling cascade.
MAP kinases MPK9 and MPK12 are preferentially expressed in guard cells and positively regulate ROS-mediated ABA signaling.
MPK12 is both a physiological substrate of IBR5 and a novel negative regulator of auxin signaling.
Study established an important role of p38gamma MAPK in epithelial-mesenchymal transition (EMT) and identified a novel signaling pathway for p38gamma MAPK-mediated tumor promotion. p38gamma MAPK regulated miR-200b through inhibiting GATA3 by inducing its ubiquitination, leading proteasome-dependent degradation.
Regulation of atypical MAP kinases ERK3 and ERK4 by the phosphatase DUSP2 has been reported.
NMR Characterization of Information Flow and Allosteric Communities in the MAP Kinase p38gamma.
study revealed a molecular pathway consisting of BMI1, miRNA let-7i, and ERK3, which controls the migration of head and neck cancer cells, and suggests that ERK3 kinase is a potential new therapeutic target in head and neck cancers, particularly those with BMI1 overexpression.
the p38gamma.PTPN4 interaction promotes cellular signaling, preventing cell death induction.
There was significant association between p38gamma expression and esophageal squamous cell carcinoma clinical stage, lymph nodes metastases, and tumor volume. p38delta overexpression can promote tumorigenesis in nude mice model xenografted with Eca109 cells whose basal level of p38delta was stably over-expressed and p38gamma was stably knocked down.
This study reveals a novel pathway that directly links ErbB4 and p38gamma to the transcriptional machinery of NKx2.5-GATA4 complex which is critical for cardiomyocyte formation during mammalian heart development.
during interphase ERK3 is mainly resident in the nucleoplasm in association with ribonuclear proteins involved in early pre-mRNA splicing, it undergoes cell cycle-dependent redistribution and, during apoptosis
Taken together our data suggest that as cells initiate adhesion to matrix increasing levels of ERK3 at the cell periphery are required to orchestrate cell morphology changes which can then drive migratory behavior.
p38gamma and p38delta reprogram liver metabolism by modulating neutrophil infiltration and provide a potential target for NAFLD therapy
analysis of how allosteric regulation of p38gamma and PTPN3 involves a PDZ domain-modulated complex formation
Thus, in endothelial cells p38alpha mediates apoptotic signaling, whereas p38beta and p38gamma transduce survival signaling
p38gamma Mitogen-activated protein kinase signals through phosphorylating its phosphatase PTPH1 in regulating ras protein oncogenesis and stress response.
SEPW1 silencing increases MKK4, which activates p38gamma, p38delta, and JNK2 to phosphorylate p53 on Ser-33 and cause a transient G(1) arrest.
phosphorylation at Ser-118 is required for ER to bind both p38gamma and c-Jun, thereby promoting ER relocation from ERE to AP-1 promoter sites.
p38gamma mitogen-activated protein kinase regulates breast cancer cell motility and metastasis, in part, by controlling expression of the metastasis-associated small GTPase RhoC.
a new paradigm in which p38gamma actively regulates the drug-Topo IIalpha signal transduction, and this may be exploited to increase the therapeutic activity of Topo II drugs.
demonstrates that p38gamma MAPK is a promising target for the design of targeted therapies for basal-like breast cancer with metastatic characteristics and for overcoming potential resistance against the PARP inhibitor
The majority of p38gamma-depleted cells die at mitotic arrest or soon after abnormal exit from M-phase.
In response to hyperosmotic stress, p38 also regulates formation of complexes between hDlg and PSF.
p38gamma mitogen-activated protein kinase mediates inflammatory signaling to promote colon tumorigenesis
p38gamma and p38delta control heart growth by modulating mTOR pathway through DEPTOR phosphorylation and subsequent degradation.
Findings provide genetic evidence that p38gamma and p38delta have essential roles in skin tumour development.
Together, our results establish that p38gamma and p38delta are central to colitis-associated colon cancer formation through regulation of hematopoietic cell response to injury, and validate p38gamma and p38kappa as potential targets for cancer therapy.
An energetic signal may trigger phosphorylation of the p38-gamma isoform which may explain how contractions differentially activate signaling pathways.
p38gamma and p38delta are crucial regulators of inflammatory joint destruction in collagen-induced arthritis.
p38gamma and p38delta kinases regulate the Toll-like receptor 4 (TLR4)-induced cytokine production by controlling ERK1/2 protein kinase pathway activation
results indicate that p38gamma and p38delta have a role in the suppression of tumor development
p38gamma contributes to the ability of cells to cope with UV exposure by regulating the checkpoint signaling pathways and the repair of damaged DNA
Results show that p38alpha is essential for myoblast differentiation, and p38gamma has a minor, yet opposing antimyogenic, function.
p38-gamma signaling directly induces the assembly of a repressive MyoD transcriptional complex.
Cardiac expression and subcellular localization
hyperactive variants of p38alpha induce, whereas hyperactive variants of p38gamma suppress, activating protein 1-mediated transcription
Mapk14 antagonizes Mapk12 activity through c-Jun-dependent ubiquitin-proteasome pathways in regulating Ras transformation and stress response.
Involvement of the p38 mitogen-activated protein kinase alpha, beta, and gamma isoforms in myogenic differentiation.
This study constitutes the first analysis addressing the functionality of p38beta, p38gamma and p38delta in satellite cell-dependent adult muscle regeneration and growth.
Activation of members of the mitogen-activated protein kinase family is a major mechanism for transduction of extracellular signals. Stress-activated protein kinases are one subclass of MAP kinases. The protein encoded by this gene functions as a signal transducer during differentiation of myoblasts to myotubes.
mitogen-activated protein kinase 12
, MAP kinase 12
, MAPK 12
, extracellular signal-regulated kinase 6
, stress-activated protein kinase 3
, MAP kinase p38 gamma
, mitogen-activated protein kinase 3
, mitogen-activated protein kinase p38 gamma
, mitogen activated protein kinase 12
, stress activated protein kinase 3
, SAP kinase-3