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ITT5739

ITT5739
ITT5739
ITT5739
  • Catalog: ITT5739
  • Gene/Protein: KRAS
  • Product Description: Immunotag™ K-Ras Polyclonal Antibody
385.0000
Price in reward points: 385

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Immunotag™ K-Ras Polyclonal Antibody
Antibody Specification
Datasheet
Target Protein K-Ras
Clonality Polyclonal
Storage/Stability -20°C/1 year
Application WB,IHC-p,ELISA
Recommended Dilution IHC-p: 100-300.Western Blot: 1/500 - 1/2000. ELISA: 1/10000. Not yet tested in other applications.
Concentration 1 mg/ml
Reactive Species Human,Mouse,Rat
Host Species Rabbit
Immunogen Synthesized peptide derived from K-Ras, at AA range: C-TERM
Specificity K-Ras Polyclonal Antibody detects endogenous levels of v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog
Purification The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen
Form Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Gene Name KRAS
Accession No. P01116 P32883 P08644
Alternate Names GTPase KRas (K-Ras 2) (Ki-Ras) (c-K-ras) (c-Ki-ras) [Cleaved into: GTPase KRas, N-terminally processed]
Description KRAS proto-oncogene, GTPase(KRAS) Homo sapiens 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. [provided by RefSeq, Jul 2008],
Cell Pathway/ Category MAPK_ERK_Growth,MAPK_G_Protein,ErbB_HER,Chemokine,Dorso-ventral axis formation,Axon guidance,VEGF,Tight junction,Gap junction,Natural killer cell mediated cytotoxicity,T_Cell_Receptor,B_Cell_Antigen,Fc epsilon RI,Long-term potentiation,Neurotrophin,Long-term depression,Regulates Actin and Cytoskeleton,Insulin_Receptor,GnRH,Progesterone-mediated oocyte maturation,Melanogenesis,Aldosterone-regulated sodium reabsorption,Pathways in cancer,Colorectal cancer,Renal cell carcinoma,Pancreatic cancer,Endometrial cancer,Glioma,Prostate cancer,Thyroid cancer,Melanoma,Bladder cancer,Chronic myeloid leukemia,Acute myeloid leukemia,Non-small cell lung cancer,
Protein Expression Brain,Cervix carcinoma,Colon carcinoma,Gallbladder tumor,Lung,Lung carcinom
Subcellular Localization intracellular,cytoplasm,mitochondrion,cytosol,plasma membrane,focal adhesion,membrane,extrinsic component of cytoplasmic side of plasma membrane,membrane raft,
Protein Function Isoforms differ in the C-terminal region which is encoded by two alternative exons (IVA and IVB),disease:Defects in KRAS are a cause of acute myelogenous leukemia (AML) [MIM:601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development.,disease:Defects in KRAS are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:115150]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant.,disease:Defects in KRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. It is characterized by leukocytosis with tissue infiltration and in vitro hypersensitivity of myeloid progenitors to granulocyte-macrophage colony stimulating factor.,disease:Defects in KRAS are the cause of Noonan syndrome 3 (NS3) [MIM:609942]. Noonan syndrome (NS) [MIM:163950] is a disorder characterized by dysmorphic facial features, short stature, hypertelorism, cardiac anomalies, deafness, motor delay, and a bleeding diathesis. It is a genetically heterogeneous and relatively common syndrome, with an estimated incidence of 1 in 1000-2500 live births. Rarely, NS is associated with juvenile myelomonocytic leukemia (JMML). NS3 inheritance is autosomal dominant.,disease:KRAS mutations are involved in cancer development.,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).,function:Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.,online information:The Singapore human mutation and polymorphism database,similarity:Belongs to the small GTPase superfamily. Ras family.,subunit:Interacts with PHLPP.,
Usage For Research Use Only! Not for diagnostic or therapeutic procedures.
Material Safety Data Sheet
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