Anti-MAPK15 polyclonal antibody (DPABH-00657)

Rabbit anti-Human MAPK15 (aa 1-245) polyclonal antibody for WB,ICC/IF,IHC-P

Specifications


Host Species
Rabbit
Antibody Isotype
IgG
Species Reactivity
Human
Immunogen
Recombinant fragment, corresponding to a region within amino acids 1-245 of Human MAPK15.
Conjugate
Unconjugated

Applications


Application Notes
WB: 1/500 - 1/3000; ICC/IF: 1/100 - 1/1000; IHC-P: 1/100 - 1/1000.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
MAPK15; mitogen-activated protein kinase 15; ERK7; ERK8; extracellular signal regulated kinase 8; ERK-7
Entrez Gene ID
UniProt ID

Citations


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References


Identification of Biological Targets of Therapeutic Intervention for Hepatocellular Carcinoma by Integrated Bioinformatical Analysis

MEDICAL SCIENCE MONITOR

Authors: Hu, Wei Qi; Wang, Wei; Fang, Di Long; Yin, Xue Feng

Background: We screened the potential molecular targets and investigated the molecular mechanisms of hepatocellular carcinoma (HCC). Material/Methods: Microarray data of GSE47786, including the 40 mu M berberine-treated HepG2 human hepatoma cell line and 0.08% DMSO-treated as control cells samples, was downloaded from the GEO database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analyses were performed; the protein-protein interaction (PPI) networks were constructed using STRING database and Cytoscape; the genetic alteration, neighboring genes networks, and survival analysis of hub genes were explored by cBio portal; and the expression of mRNA level of hub genes was obtained from the Oncomine databases. Results: A total of 56 upregulated and 8 downregulated DEGs were identified. The GO analysis results were significantly enriched in cell-cycle arrest, regulation of transcription, DNA-dependent, protein amino acid phosphorylation, cell cycle, and apoptosis. The KEGG pathway analysis showed that DEGs were enriched in MAPK signaling pathway, ErbB signaling pathway, and p53 signaling pathway. JUN, EGR1, MYC, and CDKN1A were identified as hub genes in PPI networks. The genetic alteration of hub genes was mainly concentrated in amplification. TP53, NDRG1, and MAPK15 were found in neighboring genes networks. Altered genes had worse overall survival and disease-free survival than unaltered genes. The expressions of EGR1, MYC, and CDKN1A were significantly increased, but expression of JUN was not, in the Roessler Liver datasets. Conclusions: We found that JUN, EGR1, MYC, and CDKN1A might be used as diagnostic and therapeutic molecular biomarkers and broaden our understanding of the molecular mechanisms of HCC.

MAPK15 is part of the ULK complex and controls its activity to regulate early phases of the autophagic process

JOURNAL OF BIOLOGICAL CHEMISTRY

Authors: Colecchia, David; Dapporto, Francesca; Tronnolone, Serena; Salvini, Laura; Chiariello, Mario

Autophagy, a pathway for bulk protein degradation and removal of damaged organelles, represents one of the major responses of cells to stress, thereby exerting a strict control on their correct functioning. Consequently, this process has been involved in the pathogenesis and therapeutic responses of several human diseases. Mitogen-activated protein (MAP) kinase 15 (MAPK15) is an atypical member of the MAP kinase family that recently emerged as a key modulator of autophagy and, through this, of cell transformation. Still, no information is available about signaling pathways mediating the effect of MAPK15 on this process, nor is it known which phase of autophagosome biogenesis is affected by this MAP kinase. Here, we demonstrate that MAPK15 stimulated 5-AMP-activated protein kinase-dependent activity of UNC-51-like kinase 1 (ULK1), the only protein kinase among the ATG-related proteins, toward downstream substrates and signaling intermediates. Importantly, MAPK15 directly interacted with the ULK1 complex and mediated ULK1 activation induced by starvation, a classical stimulus for the autophagic process. In turn, ULK1 and its highly homologous protein ULK2 are able to transduce MAPK15 signals stimulating early phases of autophagosomal biogenesis in a multikinase cascade that offers numerous potential targets for future therapeutic intervention in cancer and other autophagy-related human diseases.

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