Human FRS2 Recombinant Protein (N-GST & C-His) (HV168042)

Name: Human FRS2 Recombinant Protein (N-GST & C-His)
Brand: abinScience
SKU: HV168042
Price: 211 USD
Availability: InStock

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Overview

Catalog No.	HV168042
Description	Recombinant Human FRS2 Protein, N-GST & C-His (HV168042) expressed in E. coli. Purity: >90% as determined by SDS-PAGE.. Highlights ●E. coli Expression — High-yield, cost-effective production. ●High Purity — >90% as determined by SDS-PAGE.
Expression system	E. coli
Accession	Q8WU20
Protein length	Asn19-Ser109
Applications	ELISA, Immunogen, SDS-PAGE, WB, Bioactivity testing in progress
Species	Homo sapiens (Human)
Nature	Recombinant
Endotoxin level	Please contact with the lab for this information.
Purity	>90% as determined by SDS-PAGE.
Form	Lyophilized
Storage buffer	Lyophilized from a solution in PBS pH 7.4, 1 mM EDTA, 4% Trehalose, 1% Mannitol. Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.
Reconstitution	Reconstitute in sterile water for a stock solution. A copy of datasheet will be provided with the products, please refer to it for details.
Shipping	In general, proteins are provided as lyophilized powder/frozen liquid. They are shipped out with dry ice/blue ice unless customers require otherwise.
Stability and Storage	Use a manual defrost freezer and avoid repeated freeze thaw cycles. Store at 2 to 8°C for frequent use. Store at -20 to -80°C for twelve months from the date of receipt.
Alternate Names	FGFR substrate 2, FGFR-signaling adaptor SNT, FRS2, Fibroblast growth factor receptor substrate 2, SNT-1, Suc1-associated neurotrophic factor target 1
Background	Fibroblast growth factor receptor substrate 2 is a ~57 kDa protein. Adapter protein that links activated FGR and NGF receptors to downstream signaling pathways. Plays an important role in the activation of MAP kinases and in the phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, in response to ligand-mediated activation of FGFR1. Modulates signaling via SHC1 by competing for a common binding site on NTRK1.
Note	For research use only