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Unconjugated Human KRAS (G12V) Protein, His,Avitag™ (active enzyme)

AIDD‑Ready
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Menge
KRS-H51Q3-25ug
$350.00
In Stock - Delivery in 1-2 business days
KRS-H51Q3-200ug
$1,520.00
In Stock - Delivery in 2-3 weeks
KRS-H51Q3
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Synonyms

GTPase Kras, K-Ras 2, Ki-Ras, c-K-ras, c-Ki-ras, KRAS2, RASK2, C-K-RAS, CFC2, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B, KI-RAS, KRAS1, KRAS2, NS, NS3, RASK2, KRAS

Source

Unconjugated Human KRAS (G12V) Protein, His,Avitag (KRS-H51Q3) is expressed from E. coli cells. It contains AA Thr 2 - Cys 185 (Accession # P01116-2 (G12V)).

Molecular Characterization
Other Tags and Version Biotin & Other Labeled Version

This protein carries a polyhistidine tag at the N-terminus, followed by an Avi tag (Avitag™).

The protein has a calculated MW of 24.7 kDa. The protein migrates as 27 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE).

Purity

>95% as determined by SDS-PAGE.

Formulation

Supplied as 0.2 μm filtered solution in 20 mM Tris, 500 mM NaCl, pH7.5 with glycerol as protectant.

Contact us for customized product form or formulation.

Shipping and Storage

This product is supplied and shipped on dry ice.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:
  • The product MUST be stored at -70°C or lower upon receipt;
  • -70°C for 3 months under sterile conditions.
ACRO Quality Management System

Background Introduction

KRAS (Kirsten rat sarcoma 2 viral oncogene homolog) gene is a proto-oncogene that encodes a small GTPase transductor protein called KRAS. KRAS is also known as Ki-Ras, c-K-ras and c-Ki-ras. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation, promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner. RAS is one of the most frequently mutated oncogenes in human cancer but the frequency and distribution of RAS gene mutations are not uniform. In details, mutation of glycine 12 (G12) causes RAS activation by interfering with GAP binding and GAP-stimulated GTP hydrolysis. The reference shows the pathway may as a potential therapy targets.