Aliases for MRVI1 Gene
- Murine Retrovirus Integration Site 1 Homolog 2 3
- Inositol 1,4,5-Trisphosphate Receptor-Associated CGMP Kinase Substrate 3 4
- IP3R-Associated CGMP Kinase Substrate 2 3
- JAW1-Related Protein MRVI1 3 4
- JAW1L 3 4
- IRAG 3 4
- Inositol 1,4,5-Triphosphate Receptor-Associated CGMP Kinase Substrate 3
- Inositol 1,4,5-Triphosphate-Associated CGMP Kinase Substrate 2
- Protein MRVI1 3
External Ids for MRVI1 Gene
This gene is similar to a putative mouse tumor suppressor gene (Mrvi1) that is frequently disrupted by mouse AIDS-related virus (MRV). The encoded protein, which is found in the membrane of the endoplasmic reticulum, is similar to Jaw1, a lymphoid-restricted protein whose expression is down-regulated during lymphoid differentiation. This protein is a substrate of cGMP-dependent kinase-1 (PKG1) that can function as a regulator of IP3-induced calcium release. Studies in mouse suggest that MRV integration at Mrvi1 induces myeloid leukemia by altering the expression of a gene important for myeloid cell growth and/or differentiation, and thus this gene may function as a myeloid leukemia tumor suppressor gene. Several alternatively spliced transcript variants encoding different isoforms have been found for this gene, and alternative translation start sites, including a non-AUG (CUG) start site, are used. [provided by RefSeq, May 2011]
GeneCards Summary for MRVI1 Gene
MRVI1 (Murine Retrovirus Integration Site 1 Homolog) is a Protein Coding gene. Diseases associated with MRVI1 include myeloid leukemia. Among its related pathways are Platelet homeostasis and Hemostasis. An important paralog of this gene is LRMP.
UniProtKB/Swiss-Prot for MRVI1 Gene
Plays a role as NO/PRKG1-dependent regulator of IP3-induced calcium release; its phosphorylation by PRKG1 inhibits bradykinin and IP3-induced calcium release from intracellular stores. Recruits PRKG1 to the endoplasmic reticulum and may mediate the assembly of PRKG1 and ITPR1 in a macrocomplex. Involved in PRKG1 signaling cascade leading to inhibition of platelet activation and aggregation. Mediates also NO-dependent inhibition of calcium signaling in gastrointestinal smooth muscle contributing to NO-dependent relaxation.