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c-Met/Met/HGFR  Proteína

All c-Met Reagents

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10692-H03H-100
10692-H03H-200
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10692-H08H-50
10692-H08H-100
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Anfitrión de expresión: Baculovirus-Insect Cells  
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10692-H20B1-50
10692-H20B1-20
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50622-M02H-100
50622-M02H-200
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50622-M08H-100
50622-M08H-200
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80004-R02H-50
80004-R02H-100
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90304-C02H-100
90304-C02H-200
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90304-C08H-100
90304-C08H-200
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90304-CCCH-100
90304-CCCH-200
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70008-D08H-50
70008-D08H-100
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c-Met/Met/HGFR Resumen e información sobre la proteína

c-Met/Met/HGFR Información relacionada

c-Met/Met/HGFR Fondo

Resumen de gen: The proto-oncogene MET product is the hepatocyte growth factor receptor and encodes tyrosine-kinase activity. The primary single chain precursor protein is post-translationally cleaved to produce the alpha and beta subunits, which are disulfide linked to form the mature receptor. Various mutations in the MET gene are associated with papillary renal carcinoma. Two transcript variants encoding different isoforms have been found for this gene.
General information above from NCBI
Actividad catalítica: ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate.
Regulación de enzima: In its inactive state, the C-terminal tail interacts with the catalytic domain and inhibits the kinase activity. Upon ligand binding, the C-terminal tail is displaced and becomes phosphorylated, thus increasing the kinase activity.
Estructura de subunidad: Heterodimer made of an alpha chain (50 kDa) and a beta chain (145 kDa) which are disulfide linked. Binds PLXNB1. Interacts when phosphorylated with downstream effectors including STAT3, PIK3R1, SRC, PCLG1, GRB2 and GAB1. Interacts with SPSB1, SPSB2 and SPSB4 (By similarity). Interacts with INPP5D/SHIP1. When phosphorylated at Tyr-1356, interacts with INPPL1/SHIP2. Interacts with RANBP9 and RANBP10, as well as SPSB1, SPSB2, SPSB3 and SPSB4. SPSB1 binding occurs in the presence and in the absence of HGF, however HGF treatment has a positive effect on this interaction. Interacts with MUC20; prevents interaction with GRB2 and suppresses hepatocyte growth factor-induced cell proliferation. Interacts with GRB10. Interacts with PTPN1 and PTPN2.
Dominio: The kinase domain is involved in SPSB1 binding.
The beta-propeller Sema domain mediates binding to HGF.
Localización subcelular: Membrane; Single-pass type I membrane protein.
Isoform 3: Secreted.
Especificidad del tejido: Expressed in normal hepatocytes as well as in epithelial cells lining the stomach, the small and the large intestine. Found also in basal keratinocytes of esophagus and skin. High levels are found in liver, gastrointestinal tract, thyroid and kidney. Also present in the brain.
Postranslacional: Autophosphorylated in response to ligand binding on Tyr-1234 and Tyr-1235 in the kinase domain leading to further phosphorylation of Tyr-1349 and Tyr-1356 in the C-terminal multifunctional docking site. Dephosphorylated by PTPRJ at Tyr- 1349 and Tyr-1365. Dephosphorylated by PTPN1 and PTPN2.
Ubiquitinated. Ubiquitination by CBL regulates the receptor stability and activity through proteasomal degradation.
Implicación en la enfermedad: Note=Activation of MET after rearrangement with the TPR gene produces an oncogenic protein.
Note=Defects in MET may be associated with gastric cancer.
Hepatocellular carcinoma (HCC) [MIM:114550]: A primary malignant neoplasm of epithelial liver cells. The major risk factors for HCC are chronic hepatitis B virus (HBV) infection, chronic hepatitis C virus (HCV) infection, prolonged dietary aflatoxin exposure, alcoholic cirrhosis, and cirrhosis due to other causes. Note=The disease is caused by mutations affecting the gene represented in this entry.
Renal cell carcinoma papillary (RCCP) [MIM:605074]: A subtype of renal cell carcinoma tending to show a tubulo-papillary architecture formed by numerous, irregular, finger-like projections of connective tissue. Renal cell carcinoma is a heterogeneous group of sporadic or hereditary carcinoma derived from cells of the proximal renal tubular epithelium. Note=The disease is caused by mutations affecting the gene represented in this entry.
Note=A common allele in the promoter region of the MET shows genetic association with susceptibility to autism in some families. Functional assays indicate a decrease in MET promoter activity and altered binding of specific transcription factor complexes.
Note=MET activating mutations may be involved in the development of a highly malignant, metastatic syndrome known as cancer of unknown primary origin (CUP) or primary occult malignancy. Systemic neoplastic spread is generally a late event in cancer progression. However, in some instances, distant dissemination arises at a very early stage, so that metastases reach clinical relevance before primary lesions. Sometimes, the primary lesions cannot be identified in spite of the progresses in the diagnosis of malignancies.
Similitud de la secuencia: Belongs to the protein kinase superfamily. Tyr protein kinase family.
Contains 3 IPT/TIG domains.
Contains 1 protein kinase domain.
Contains 1 Sema domain.
General information above from UniProt

Hepatocyte growth factor receptor (HGFR), also known as c-Met or mesenchymal-epithelial transition factor (MET), is a receptor tyrosine kinase (RTK) that has been shown to be overexpressed and/or mutated in a variety of malignancies. HGFR protein is produced as a single-chain precursor, and HGF is the only known ligand. Normal HGF/HGFR signaling is essential for embryonic development, tissue repair or wound healing, whereas aberrantly active HGFR has been strongly implicated in tumorigenesis, particularly in the development of invasive and metastatic phenotypes. HGFR protein is a multifaceted regulator of growth, motility, and invasion, and is normally expressed by cells of epithelial origin. Preclinical studies suggest that targeting aberrant HGFR signaling could be an attractive therapy in cancer.

c-Met/Met/HGFR Nombre alternativo

c-Met/Met/HGFR Estudios relacionados

  • McGill GG, et al. (2006) c-Met expression is regulated by Mitf in the melanocyte lineage. J Biol Chem. 281(15): 10365-73.
  • Garcia S, et al. (2007) c-Met overexpression in inflammatory breast carcinomas: automated quantification on tissue microarrays. British journal of cancer. 96(2): 329-35.
  • Socoteanu MP, et al. (2008) c-Met targeted therapy of cholangiocarcinoma. World J Gastroenterol. 14(19): 2990-4.
  • Kong DS, et al. (2009) Prognostic significance of c-Met expression in glioblastomas. Cancer. 115(1): 140-8.
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