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Die folgenden MAPmates™ sollten nicht zusammen analysiert werden: -MAPmates™, die einen unterschiedlichen Assaypuffer erfordern. -Phosphospezifische und MAPmate™ Gesamtkombinationen wie Gesamt-GSK3β und Gesamt-GSK3β (Ser 9). -PanTyr und locusspezifische MAPmates™, z.B. Phospho-EGF-Rezeptor und Phospho-STAT1 (Tyr701). -Mehr als 1 Phospho-MAPmate™ für ein einziges Target (Akt, STAT3). -GAPDH und β-Tubulin können nicht mit Kits oder MAPmates™, die panTyr enthalten, analysiert werden.
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48-602MAG
Buffer Detection Kit for Magnetic Beads
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This Anti-c-K-Ras Antibody, clone 234-4.2 is validated for use in Western Blotting, IHC for the detection of c-K-Ras.
More>>This Anti-c-K-Ras Antibody, clone 234-4.2 is validated for use in Western Blotting, IHC for the detection of c-K-Ras. Less<<
Anti-c-K-Ras Antibody, clone 234-4.2: SDB (Sicherheitsdatenblätter), Analysenzertifikate und Qualitätszertifikate, Dossiers, Broschüren und andere verfügbare Dokumente.
GTPase KRas (c-k-ras; K-ras) is a membrane-bound G protein belonging to the family of Ras GTPases. They are activated by the binding of GTP in response to signals from various receptors including the epidermal growth factor receptor (EGFR). Ras GTPases are regulated by guanine nucleotide exchange factors (GEF) and GTPase activating proteins (GAP) and lie upstream of the MAP kinase pathway which controls a range of cellular processes including proliferation and differentiation. Previous studies have suggested that KRas plays an important role in embryonic development, and it may also contribute to the pathogenesis of colorectal cancer via an EGFR-mediated pathway.
References
Product Information
Format
Purified
Control
SW-480 cell lysate
Presentation
Purified mouse monoclonal IgG2aκ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
This Anti-c-K-Ras Antibody, clone 234-4.2 is validated for use in Western Blotting, IHC for the detection of c-K-Ras.
Key Applications
Western Blotting
Immunohistochemistry
Application Notes
Western Blot Analysis: A representative lot detected c-K-Ras in A431 cell lysate.
Western Blot Analysis: A representative lot from an independent laboratory detected c-K-Ras in primary human lymphoid leukemia cell lysates, and in normal and HA-dynamin K44A mutant HeLa cell lysates (Omerovic, J., et al. (2008). Oncogene. 27(19):2754-2762.).
Immunohistochemistry Analysis: A representative lot from an independent laboratory detected c-K-Ras in non-small cell lung cancer cells (Volm, M., et al. (2002). Clin Cancer Res. 8(6):1843-1848.).
Biological Information
Immunogen
Recombinant protein corresponding to rat c-K-Ras.
Clone
234-4.2
Host
Mouse
Isotype
IgG2aκ
Species Reactivity
Human
Species Reactivity Note
Demonstrated to react with Human. Predicted to react with Rat based on immunogen design.
FUNCTION: Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
ENZYME REGULATION: Alternate between an inactive form bound to GDP and an active form bound to GTP. Activated by a guanine nucleotide-exchange factor (GEF) and inactivated by a GTPase-activating protein (GAP).
SUBUNIT STRUCTURE: Interacts with PHLPP. Interacts (active GTP-bound form preferentially) with RGS14.
SEQUENCE SIMILARITIES: Belongs to the small GTPase superfamily. Ras family.
Molecular Weight
~22 kDa observed
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blot in SW-480 cell lysate.
Western Blot Analysis: 1 µg/mL of this antibody detected c-K-Ras in 10 µg of SW-480 cell lysate.
Usage Statement
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
The ubiquitously expressed major Ras isoforms: H-, K- and N-Ras, are highly conserved, yet exhibit different biological outputs. We have compared the relative efficiencies with which epidermal or hepatocyte growth factor activates Ras isoforms and the requirement for specific isoforms in the activation of downstream pathways. We find that the relative coupling efficiencies to each Ras isoform are conserved between stimuli. Furthermore, in both cases, inhibition of receptor endocytosis led to reduced N- and H-Ras activation, but K-Ras was unaffected. Acute knockdown of each isoform with siRNA allows endogenous Ras isoform function and abundance to be probed. This revealed that there is significant variation in the contribution of individual isoforms to total Ras across a panel of cancer cell lines although typically K> or =N>H. Intriguingly, cancer cell lines where a significant fraction of endogenous Ras is oncogenically mutated showed attenuated activation of canonical Ras effector pathways. We profiled the contribution of each Ras isoform to the total Ras pool allowing interpretation of the effect of isoform-specific knockdown on signalling outcomes. In contrast to previous studies indicating preferential coupling of isoforms to Raf and PtdIns-3-kinase pathways, we find that endogenous Ras isoforms show no specific coupling to these major Ras pathways.
Expression profile of genes in non-small cell lung carcinomas from long-term surviving patients. Volm, Manfred, et al. Clin. Cancer Res., 8: 1843-8 (2002)
2002
Non-small cell lung cancer (NSCLC) is usually associated with a poor prognosis. Some patients survive their disease, and the underlying molecular mechanisms are still poorly understood. The purpose of this investigation was to evaluate expression profiles of proteins determining the survival of NSCLC patients for 5 years.