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activity; localization, and function is regulated by the C-terminal tail. Additionally we are shipping Mitogen-Activated Protein Kinase 15 Kits (9) and Mitogen-Activated Protein Kinase 15 Proteins (7) and many more products for this protein.
Showing 10 out of 84 products:
Human Polyclonal MAPK15 Primary Antibody for EIA, IHC (p) - ABIN359709
Klevernic, Stafford, Morrice, Peggie, Morton, Cohen: Characterization of the reversible phosphorylation and activation of ERK8. in The Biochemical journal 2006
Show all 4 references for ABIN359709
Human Polyclonal MAPK15 Primary Antibody for IF, WB - ABIN2786203
Saelzler, Spackman, Liu, Martinez, Harris, Abe: ERK8 down-regulates transactivation of the glucocorticoid receptor through Hic-5. in The Journal of biological chemistry 2006
Human Polyclonal MAPK15 Primary Antibody for IHC (p), WB - ABIN391796
Groehler, Lannigan: A chromatin-bound kinase, ERK8, protects genomic integrity by inhibiting HDM2-mediated degradation of the DNA clamp PCNA. in The Journal of cell biology 2010
CapZIP (show RCSD1 Antibodies), which has been shown to regulate ciliogenesis, is an ERK7 substrate, and that Dishevelled (show DVL2 Antibodies), which has also been shown to regulate ciliogenesis, facilitates ERK7 phosphorylation of CapZIP (show RCSD1 Antibodies) through binding to both ERK7 and CapZIP (show RCSD1 Antibodies).
In HeLa cells, phosphorylation of HuR (show ELAVL1 Antibodies) by ERK8 prevents it from binding to PDCD4 (show PDCD4 Antibodies) mRNA and allows miR (show MLXIP Antibodies)-21-mediated degradation of PDCD4 (show PDCD4 Antibodies).
depletion of endogenous MAPK15 expression inhibited BCR (show BCR Antibodies)-ABL1 (show ABL1 Antibodies)-dependent cell proliferation, in vitro
The present study suggests that MAPK15 overexpression may contribute to the malignant transformation of gastric mucosa by prolonging the stability of c-Jun (show JUN Antibodies).
ERK8 appears as a constitutive brake on N-Acetylgalactosaminyltransferase (show B4GALNT2 Antibodies) relocalisation, and the loss of its expression could drive cancer aggressivity through increased cell motility.
Data suggest that the model coulb be a tool for the development of specific ERK8 kinase inhibitors.
ATG8 (show GABARAPL2 Antibodies)-like proteins (MAP1LC3B (show MAP1LC3B Antibodies), GABARAP (show GABARAP Antibodies) and GABARAPL1 (show GABARAPL1 Antibodies)) are novel interactors of MAPK15/ERK8, a MAP kinase (show MAPK1 Antibodies) involved in cell proliferation and transformation.
a novel function for ERK8 as a bona fide ERRalpha (show ESRRA Antibodies) corepressor, involved in control of its cellular localization by nuclear exclusion, and suggest a key role for this MAP kinase (show MAPK1 Antibodies) in the regulation of the biological activities of this nuclear receptor.
Data show that ERK8 prevents HDM2-mediated PCNA (show PCNA Antibodies) destruction by inhibiting the association of PCNA (show PCNA Antibodies) with HDM2, and implicate ERK8 in the regulation of genomic stability.
Extracellular signal-regulated kinase 8-mediated c-Jun (show JUN Antibodies) phosphorylation increases tumorigenesis of human colon cancer
ERK8, a new member of the mitogen-activated protein kinase (show MAPK1 Antibodies) family.
Taken together, our results suggest that ERK8 plays an important role in spindle organization during mouse oocyte meiotic maturation and early embryo cleavage.
Erk8 has a role as a novel effector of RET (show RET Antibodies)/PTC3 (show NCOA4 Antibodies) and, therefore, RET (show RET Antibodies) biological functions
activity\; localization, and function is regulated by the C-terminal tail
mitogen-activated protein kinase 15
, extracellular signal-regulated kinase 7
, MAP kinase 15
, MAPK 15
, extracellular regulated kinase 8 delta
, extracellular signal regulated kinase 8
, extracellular signal-regulated kinase 8