KIT / c-KIT recombinant protein

Recombinant Rat KIT / c-KIT Protein (His tag)

Cat. Num. AAA2547348

• Purity: > 95 % as determined by SDS-PAGE
• Synonyms: KIT / c-KIT; Recombinant Rat KIT / c-KIT Protein (His tag); KIT; KIT / c-KIT recombinant protein

• Host: Human Cells
• Purity/Purification: > 95 % as determined by SDS-PAGE
• Form/Format: Lyophilized from sterile PBS, pH 7.4
• Sequence Length: 978

• Application Notes: The recombinant rat KIT comprises 509 amino acids and predicts a molecular mass of 56.9 kDa. The apparent molecular mass of the recombinant protein is approximately 83 kDa in SDS-PAGE under reducing conditions due to glycosylation.
• Predicted N Terminal: Ser 25
• Endotoxin: < 1.0 EU per mug of the protein as determined by the LAL method
• Preparation and Storage: Samples are stable for up to twelve months from date of receipt at -70 degree C

SDS-PAGE

Related Product Information for KIT / c-KIT recombinant protein

Background: C-Kit is a type 3 transmembrane receptor for MGF (mast cell growth factor, also known as stem cell factor). c-Kit contains 5 Ig-like C2-type (immunoglobulin-like) domains.and 1 protein kinase domain. It belongs to the protein kinase superfamily, tyr protein kinase family and CSF-1/PDGF receptor subfamily. C-Kit contains 5 Ig-like C2-type (immunoglobulin-like) domains and 1 protein kinase domain. C-Kit has a tyrosine-protein kinase activity. Binding of the ligands leads to the autophosphorylation of KIT and its association with substrates such as phosphatidylinositol 3-kinase. Antibodies to c-Kit are widely used in immunohistochemistry to help distinguish particular type s of tumour in histological tissue sections. It is used primarily in the identification of GISTs. In GISTs, c-Kit staining is typically cytoplasmic, with stronger accentuation along the cell membranes. C-Kit antibodies can also be used in the identification of mast cell tumours and in distinguishing seminomas from embryonal carcinomas. Mutations in c-Kit gene are associated with gastrointestinal stromal tumors, mast cell disease, acute myelogenous lukemia, and piebaldism. Defects in KIT are a cause of acute myelogenous leukemia (AML). AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development. Note=Somatic mutations that lead to constitutive activation of KIT are detected in AML patients.

Description: A DNA sequence encoding the rat KIT (Q63116) (Met1-Thr522) was expressed, fused with a polyhistidine tag at the C-terminus.

NCBI and Uniprot Product Information

• NCBI GI #: 11560079
• NCBI GeneID: 64030
• NCBI Accession #: NP_071600.1
• NCBI GenBank Nucleotide #: NM_022264.1
• UniProt Accession #: Q63116
• Molecular Weight: 109,342 Da
• NCBI Official Full Name: mast/stem cell growth factor receptor Kit
• NCBI Official Synonym Full Names: KIT proto-oncogene receptor tyrosine kinase
• NCBI Official Symbol: Kit
• NCBI Protein Information: mast/stem cell growth factor receptor Kit
• UniProt Protein Name: Tyrosine-protein kinase receptor
• UniProt Gene Name: Kit

NCBI Description

transmembrane receptor; deletion mutation is associated with anemia and deficiency in mast cells and melanocytes in the Ws mutant allele of rats [RGD, Feb 2006]

Uniprot Description

Kit: a receptor tyrosine kinase and a member of the subfamily that includes PDGF, CSF-1 and FLT-3/flk-2 receptors. Receptor for stem cell factor. Plays a critical role in hematopoietic stem cell, mast cell, melanocyte and germ cell development. Ligand binding induces autophosphorylation, dimerization and activation, leading to the recruitment and phosphorylation of downstream SH2-containing signaling components including PLC-gamma, PI3 kinase p85, SHP2 and CrkL, linking c-Kit to various cell signaling pathways. Molecular lesions that impair the kinase activity of c-Kit are associated with a variety of developmental disorders, while mutations that constitutively activate c-Kit can lead to hyperplasia and tumorigenesis. Activating mutations cause >90% of gastrointestinal stromal tumors (GIST); successfully treated with inhibitors Gleevec (imatinib, Glivec) and Sutent (Sutinib, SU11248). Activating mutations also induce mastocytosis. Autocrine/paracrine stimulation may drive some lung and other tumors. Loss of expression associated with melanoma progression. Familial loss of function mutations cause piebaldism, with defects in hair and skin pigmentation due to lack of melanocytes.

Protein type: EC 2.7.10.1; Kinase, protein; Membrane protein, integral; Oncoprotein; PDGFR family; Protein kinase, TK; Protein kinase, tyrosine (receptor); TK group

Chromosomal Location of Human Ortholog: 14p11

Cellular Component: acrosome; cell surface; cytoplasm; external side of plasma membrane; extracellular space; intercellular junction; internal side of plasma membrane

Molecular Function: cytokine binding; protease binding; protein homodimerization activity; protein-tyrosine kinase activity; stem cell factor receptor activity; transmembrane receptor protein tyrosine kinase activity

Biological Process: actin cytoskeleton reorganization; activation of MAPK activity; cytokine and chemokine mediated signaling pathway; dendritic cell cytokine production; detection of mechanical stimulus involved in sensory perception of sound; embryonic hemopoiesis; epithelial cell proliferation; erythrocyte differentiation; germ cell migration; germ cell programmed cell death; glycosphingolipid metabolic process; gut development; hemopoiesis; immature B cell differentiation; inflammatory response; lamellipodium biogenesis; lymphoid progenitor cell differentiation; male gonad development; mast cell chemotaxis; mast cell cytokine production; mast cell degranulation; melanocyte differentiation; myeloid leukocyte differentiation; myeloid progenitor cell differentiation; negative regulation of programmed cell death; ovarian follicle development; peptidyl-tyrosine phosphorylation; pigmentation; pigmentation during development; positive regulation of cell migration; positive regulation of cell proliferation; positive regulation of JAK-STAT cascade; positive regulation of long-term neuronal synaptic plasticity; positive regulation of MAP kinase activity; positive regulation of MAPKKK cascade; positive regulation of Notch signaling pathway; positive regulation of pseudopodium formation; positive regulation of transcription factor activity; positive regulation of tyrosine phosphorylation of Stat1 protein; positive regulation of tyrosine phosphorylation of Stat3 protein; positive regulation of tyrosine phosphorylation of Stat5 protein; protein amino acid autophosphorylation; protein amino acid phosphorylation; regulation of cell shape; regulation of pigmentation during development; response to radiation; somatic stem cell division; somatic stem cell maintenance; spermatid development; spermatogenesis; stem cell differentiation; T cell differentiation; visual learning