Recombinant human GST-KIF5B-Ret fusion protein (Active)
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Recombinant human GST-KIF5B-Ret fusion protein (Active) is a Human Fragment protein, in the 1 to 575 aa range, expressed in Baculovirus infected Sf9 cells, with >75%, suitable for SDS-PAGE, FuncS.
View Alternative Names
CDHF12, CDHR16, PTC, RET, RET51, Proto-oncogene tyrosine-protein kinase receptor Ret, Cadherin family member 12, Proto-oncogene c-Ret, KNS, KNS1, KIF5B, Kinesin-1 heavy chain, Conventional kinesin heavy chain, Ubiquitous kinesin heavy chain, UKHC
- FuncS
Supplier Data
Functional Studies - Recombinant human GST-KIF5B-Ret fusion protein (Active) (AB268707)
The specific activity was determined to be 49.5 nmol/min/mg in a kinase assay using Poly (4 : 1 Glu, Tyr) peptide substrate.
- SDS-PAGE
Supplier Data
SDS-PAGE - Recombinant human GST-KIF5B-Ret fusion protein (Active) (AB268707)
SDS-PAGE analysis of ab268707.
Reactivity data
Sequence info
Properties and storage information
Shipped at conditions
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Aliquoting information
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
The formation of the KIF5B-RET fusion results in a constitutively active tyrosine kinase leading to unregulated cell signaling. KIF5B-RET is not known to be part of a larger stable protein complex but it initiates signaling pathways essential for cell proliferation and differentiation. The fusion protein hijacks the motor function of KIF5B to position RET inappropriately within the cell which leads to constitutive activation of downstream signaling cascades.
Pathways
The constitutive activity of the KIF5B-RET fusion protein impacts the MAPK (mitogen-activated protein kinase) and PI3K-AKT (phosphoinositide 3-kinase/protein kinase B) signaling pathways. These pathways are critical for regulating cell growth and survival and the KIF5B-RET fusion protein abnormally stimulates them. The natural RET protein associates with ligands such as GDNF (glial cell-derived neurotrophic factor) but the fusion bypasses the need for these ligands resulting in active signaling independent of external cues.
Specifications
Form
Liquid
Additional notes
Affinity purified.
General info
Function
Receptor tyrosine-protein kinase involved in numerous cellular mechanisms including cell proliferation, neuronal navigation, cell migration, and cell differentiation in response to glia cell line-derived growth family factors (GDNF, NRTN, ARTN, PSPN and GDF15) (PubMed : 20064382, PubMed : 20616503, PubMed : 20702524, PubMed : 21357690, PubMed : 21454698, PubMed : 24560924, PubMed : 28846097, PubMed : 28846099, PubMed : 28953886, PubMed : 31118272). In contrast to most receptor tyrosine kinases, RET requires not only its cognate ligands but also coreceptors, for activation (PubMed : 21994944, PubMed : 23333276, PubMed : 28846097, PubMed : 28846099, PubMed : 28953886). GDNF ligands (GDNF, NRTN, ARTN, PSPN and GDF15) first bind their corresponding GDNFR coreceptors (GFRA1, GFRA2, GFRA3, GFRA4 and GFRAL, respectively), triggering RET autophosphorylation and activation, leading to activation of downstream signaling pathways, including the MAPK- and AKT-signaling pathways (PubMed : 21994944, PubMed : 23333276, PubMed : 24560924, PubMed : 25242331, PubMed : 28846097, PubMed : 28846099, PubMed : 28953886). Acts as a dependence receptor via the GDNF-GFRA1 signaling : in the presence of the ligand GDNF in somatotrophs within pituitary, promotes survival and down regulates growth hormone (GH) production, but triggers apoptosis in absence of GDNF (PubMed : 20616503, PubMed : 21994944). Required for the molecular mechanisms orchestration during intestine organogenesis via the ARTN-GFRA3 signaling : involved in the development of enteric nervous system and renal organogenesis during embryonic life, and promotes the formation of Peyer's patch-like structures, a major component of the gut-associated lymphoid tissue (By similarity). Mediates, through interaction with GDF15-receptor GFRAL, GDF15-induced cell-signaling in the brainstem which triggers an aversive response, characterized by nausea, vomiting, and/or loss of appetite in response to various stresses (PubMed : 28846097, PubMed : 28846099, PubMed : 28953886). Modulates cell adhesion via its cleavage by caspase in sympathetic neurons and mediates cell migration in an integrin (e.g. ITGB1 and ITGB3)-dependent manner (PubMed : 20702524, PubMed : 21357690). Also active in the absence of ligand, triggering apoptosis through a mechanism that requires receptor intracellular caspase cleavage (PubMed : 21357690). Triggers the differentiation of rapidly adapting (RA) mechanoreceptors (PubMed : 20064382). Involved in the development of the neural crest (By similarity). Regulates nociceptor survival and size (By similarity). Phosphorylates PTK2/FAK1 (PubMed : 21454698).. Isoform 1. Isoform 1 in complex with GFRAL induces higher activation of MAPK-signaling pathway than isoform 2 in complex with GFRAL.
Sequence similarities
Belongs to the protein kinase superfamily. Tyr protein kinase family.
Post-translational modifications
Autophosphorylated on C-terminal tyrosine residues upon ligand stimulation.. Proteolytically cleaved by caspase-3. The soluble RET kinase fragment is able to induce cell death. The extracellular cell-membrane anchored RET cadherin fragment accelerates cell adhesion in sympathetic neurons.
Subcellular localisation
Endosome membrane
Target data
Additional targets
Product promise
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