NP_001164023.1
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NCBI GenBank Nucleotide #
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UniProt Primary Accession #
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UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
83,982 Da
NCBI Official Full Name
krev interaction trapped protein 1 isoform 2
NCBI Official Synonym Full Names
KRIT1, ankyrin repeat containing
NCBI Official Synonym Symbols
Ccm1; AA432855; AI450393; AI643869; BB155247; BB235701; 2010007K12Rik; A630036P20Rik [Similar Products]
NCBI Protein Information
krev interaction trapped protein 1; krev interaction trapped 1; cerebral cavernous malformations 1 protein homolog
UniProt Protein Name
Krev interaction trapped protein 1
UniProt Synonym Protein Names
Cerebral cavernous malformations 1 protein homolog
UniProt Synonym Gene Names
UniProt Entry Name
KRIT1_MOUSE
UniProt Comments for KRIT1
KRIT1: Component of the CCM signaling pathway which is a crucial regulator of heart and vessel formation and integrity. Negative regulator of angiogenesis. Inhibits endothelial proliferation, apoptosis, migration, lumen formation and sprouting angiogenesis in primary endothelial cells. Promotes AKT phosphorylation in a NOTCH-dependent and independent manner, and inhibits EKR1/2 phosphorylation indirectly through activation of the DELTA-NOTCH cascade. Acts in concert with CDH5 to establish and maintain correct endothelial cell polarity and vascular lumen and these effects are mediated by recruitment and activation of the Par polarity complex and RAP1B. Required for the localization of phosphorylated PRKCZ, PARD3, TIAM1 and RAP1B to the cell junction, and cell junction stabilization. Plays an important role in the maintenance of the intracellular reactive oxygen species (ROS) homeostasis to prevent oxidative cellular damage. Regulates the homeostasis of intracellular ROS through an antioxidant pathway involving FOXO1 and SOD2. Facilitates the down-regulation of cyclin-D1 (CCND1) levels required for cell transition from proliferative growth to quiescence by preventing the accumulation of intracellular ROS through the modulation of FOXO1 and SOD2 levels. Defects in KRIT1 are the cause of cerebral cavernous malformations type 1 (CCM1). Cerebral cavernous malformations (CCMs) are congenital vascular anomalies of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. CCMs have an incidence of 0.1%-0.5% in the general population and usually present clinically during the 3rd to 5th decade of life. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters. 3 isoforms of the human protein are produced by alternative splicing.
Protein type: G protein regulator, misc.; Motility/polarity/chemotaxis
Cellular Component: extracellular space; microtubule; protein complex; cytoskeleton; membrane; cell; cytoplasm; plasma membrane; intercellular junction; cell junction
Molecular Function: protein binding; phosphatidylinositol-4,5-bisphosphate binding; microtubule binding; protein complex binding; GTPase regulator activity
Biological Process: negative regulation of angiogenesis; positive regulation of protein binding; regulation of catalytic activity; cell redox homeostasis; negative regulation of endothelial cell proliferation; angiogenesis
Research Articles on KRIT1
Precautions
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Pathways associated with KRIT1 elisa kit
Diseases associated with KRIT1 elisa kit
Organs/Tissues associated with KRIT1 elisa kit
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