Aliases for MAPK8IP1 Gene
External Ids for MAPK8IP1 Gene
Previous HGNC Symbols for MAPK8IP1 Gene
Previous GeneCards Identifiers for MAPK8IP1 Gene
This gene encodes a regulator of the pancreatic beta-cell function. It is highly similar to JIP-1, a mouse protein known to be a regulator of c-Jun amino-terminal kinase (Mapk8). This protein has been shown to prevent MAPK8 mediated activation of transcription factors, and to decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes. [provided by RefSeq, May 2011]
GeneCards Summary for MAPK8IP1 Gene
MAPK8IP1 (Mitogen-Activated Protein Kinase 8 Interacting Protein 1) is a Protein Coding gene. Diseases associated with MAPK8IP1 include Diabetes Mellitus, Noninsulin-Dependent and Cervix Small Cell Carcinoma. Among its related pathways are Akt Signaling and Reelin signaling pathway. GO annotations related to this gene include identical protein binding and kinesin binding. An important paralog of this gene is MAPK8IP2.
UniProtKB/Swiss-Prot for MAPK8IP1 Gene
The JNK-interacting protein (JIP) group of scaffold proteins selectively mediates JNK signaling by aggregating specific components of the MAPK cascade to form a functional JNK signaling module. Required for JNK activation in response to excitotoxic stress. Cytoplasmic MAPK8IP1 causes inhibition of JNK-regulated activity by retaining JNK in the cytoplasm and inhibiting JNK phosphorylation of c-Jun. May also participate in ApoER2-specific reelin signaling. Directly, or indirectly, regulates GLUT2 gene expression and beta-cell function. Appears to have a role in cell signaling in mature and developing nerve terminals. May function as a regulator of vesicle transport, through interactions with the JNK-signaling components and motor proteins (By similarity). Functions as an anti-apoptotic protein and whose level seems to influence the beta-cell death or survival response.