KRAS Antibody (C-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, FC, IF, E |
---|---|
Primary Accession | P01116 |
Other Accession | P08644, P32883, NP_203524.1, NP_004976.2 |
Reactivity | Human, Mouse, Rat |
Predicted | Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 21656 Da |
Antigen Region | 146-174 aa |
Gene ID | 3845 |
---|---|
Other Names | GTPase KRas, K-Ras 2, Ki-Ras, c-K-ras, c-Ki-ras, GTPase KRas, N-terminally processed, KRAS, KRAS2, RASK2 |
Target/Specificity | This KRAS antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 146-174 amino acids from the C-terminal region of human KRAS. |
Dilution | IF~~1:10~50 WB~~1:2000 FC~~1:10~50 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | KRAS Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | KRAS |
---|---|
Synonyms | KRAS2, RASK2 |
Function | Ras proteins bind GDP/GTP and possess intrinsic GTPase activity (PubMed:20949621). Plays an important role in the regulation of cell proliferation (PubMed:22711838, PubMed:23698361). Plays a role in promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner (PubMed:24623306). |
Cellular Location | Cell membrane; Lipid-anchor; Cytoplasmic side. Endomembrane system. Cytoplasm, cytosol |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene, a Kirsten ras oncogene homolog from the mammalian ras gene family, encodes a protein that is a member of the small GTPase superfamily. A single amino acid substitution is responsible for an activating mutation. The transforming protein that results is implicated in various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas and colorectal carcinoma. Alternative splicing leads to variants encoding two isoforms that differ in the C-terminal region.
References
Bruckman, K.C., et al. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 110(5):632-637(2010)
Wong, K.K., et al. Am. J. Pathol. 177(4):1611-1617(2010)
Irahara, N., et al. Diagn. Mol. Pathol. 19(3):157-163(2010)
Carotenuto, P., et al. Pharmacogenomics 11(8):1169-1179(2010)
Leventopoulos, G., et al. Clin. Exp. Rheumatol. 28(4):556-557(2010)
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