SANTA CRUZ BIOTECHNOLOGY, INC.
K-Ras-2B (C-19): sc-521
The Power to Question
BACKGROUND
APPLICATIONS
The mammalian c-H-, c-K- and N-Ras proto-oncogenes encode 21 kDa proteins that are ubiquitously expressed in vertebrate cells. c-H- and c-K-Ras
are cellular homologs of the v-H- and v-K-Ras sequences originally isolated
form the Harvey and Kirsten strains of rat sarcoma virus. p21Ras-encoded
proteins bind GDP and GTP with high affinity and possess a low level intrinsic GTPase activity that can be stimulated over 100-fold by interaction with
cytosolic GTPase activating protein (GAP), a potential effector for Ras p21
function. Point mutations at amino acids 12, 13, 59 and 61 within domains
responsible for GTP binding and hydrolysis activate Ras proteins to their
oncogenic form and block the ability of their GTP as activities to be stimulated by GAP. The Raf protein kinase has been identified as a downstream
effector of Ras, which is regulated by 14-3-3 proteins and in turn phosphorylates and activates MAP kinases.
K-Ras-2B (C-19) is recommended for detection of K-Ras-2B p21 of mouse,
rat and human origin by Western Blotting (starting dilution 1:200, dilution
range 1:100-1:1000), immunoprecipitation [1–2 µg per 100–500 µg of total
protein (1 ml of cell lysate)] and immunofluorescence (starting dilution 1:50,
dilution range 1:50-1:500).
Molecular Weight of K-Ras-2B: 21 kDa
Positive Controls: HeLa whole cell lysate: sc-2200 or WI 38 whole cell
lysate.
DATA
203 K –
118 K –
86 K –
REFERENCES
52 K –
1. Freed, E., et al. 1994. Binding of 14-3-3 proteins to the protein kinase Raf
and effects on its activation. Science 265: 1713-1716.
35 K –
29 K –
2. Fu, H., et al. 1994. Interaction of the protein kinase Raf-1 with 14-3-3 proteins. Science 266: 126-129.
3. Cales, C., et al. 1988. The cytoplasmic protein GAP is implicated as the
target for regulation by the ras gene product. Nature 332: 548-551.
4. Adari, H., et al. 1988. Guanosine triphosphatase activating protein (GAP)
interacts with the p21 ras effector binding domain. Science 240: 518-521.
5. Barbacid, M. 1987. ras genes. Annu. Rev. Biochem. 56: 779-827.
6. Trahey, M. et al. 1987. A cytoplasmic protein stimulates normal N-ras p21
GTPase, but does not affect oncogenic mutants. Science 238: 542-545.
7. Ellis, R.W., et al. 1981. The p21 src genes of Harvey and Kirsten sarcoma
viruses originate from divergent members of a family of normal vertebrate
genes. Nature 292: 506-511.
8. Shih, T.Y., et al. 1980. Guanine nucleotide-binding and autophosphorylating activities associated with the p21src protein of Harvey murine sarcoma virus. Nature 287: 686-691.
20 K –
< K-Ras-2B
K-Ras-2B(F234): sc-521. Western blot analysis of K-Ras2B expression in KNRK whole cell lysate.
K-Ras-2B (C-19): sc-521. Immunofluorescence staining of
methanol-fixed HeLa cells showing cytoplasmic staining.
SELECT PRODUCT CITATIONS
1. Villalonga, P., et al. 2001. Calmodulin binds to K-Ras, but not to H- or NRas, and modulates its downstream signaling. Mol. Cell. Biol. 21:
7345-7354.
2. Chiloeches, A., et al. 1999. Regulation of Ras·GTP Loading and Ras-Raf
Association in Neonatal Rat Ventricular Myocytes by G Protein- coupled
Receptor Agonists and Phorbol Ester. J. Biol. Chem. 274: 19762-19770.
3. Sun, J., et al. 1998. Both farnesyltransferase and geranyltransferase I
inhibitors are required for inhibition of oncogenic K-Ras prenylation but
each alone is sufficient to suppress human tumor growth in nude mouse
xenographs. Oncogene. 16: 1467-1473.
CHROMOSOMAL LOCATION
4. Fan, J., et al. 1997. K-ras modulates the cell cycle via both positive and
negative regulatory pathways. Oncogene. 14: 2595-2607.
Genetic locus: K-ras (human) mapping to 12p12.1; K-ras (mouse) mapping
to 6 G2.
5. Pells, S., et al. 1997. Developmentally regulated expression of murine Kras isoforms. Oncogene. 15: 1781-1786.
SOURCE
STORAGE
K-Ras-2B (C-19) is an affinity purified rabbit polyclonal antibody raised
against a peptide mapping at the C-terminus of K-Ras-2B of human origin.
Store at 4° C, **DO NOT FREEZE**. Stable for one year from the date of
shipment. Non-hazardous. No MSDS required.
PRODUCT
RESEARCH USE
Each vial contains 200 µg IgG in 1.0 ml of PBS with < 0.1% sodium azide and
0.1% gelatin.
For research use only, not for use in diagnostic procedures.
Blocking peptide available for competition studies, sc-521 P, (100 µg peptide
in 0.5 ml PBS containing < 0.1% sodium azide and 0.2% BSA).
Santa Cruz Biotechnology, Inc.
1.800.457.3801
831.457.3800
fax 831.457.3801
Europe
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