K-Ras antibody

Antigen: K-Ras

Clonality: Polyclonal

Host: Rabbit

Reactivity: Human, Mouse (Murine), Rat (Rattus)

Application: Western Blotting (WB), ELISA, Immunoprecipitation (IP), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Immunohistochemistry (Formalin-fixed Sections) (IHC (f)), Flow Cytometry (FACS), Immunofluorescence (IF)

Catalog no.: ABIN736671

Additional Information

Alternative name: KRAS

Immunogen: Polyclonal antibodies are produced by immunizing animals with synthetic peptide derived from human K-ras N-terminus

Format: Lyophilized

Reconstitution: Reconstitute with 100ul sterille distilled water. After reconstitution, stock concentration=1ug/1ul, preservatives included (BSA=10ug/ul, Sodium azide=0.1%)

Isotype: IgG  (Matching secondary antibodies)

Description: Synonym: C-K-RAS, c-Ki-ras, c-Ki-ras p21, Ha-ras, K-RAS B, K-RAS2A, K-RAS2B, K-RAS4A, KI-RAS, KI-RAS4B, KRAS, KRAS1, KRAS2, MGC7141, NS, NS3, p21, p21B, p21ras, RAS, RAS1, RASH, RASK2.

Molecular Weight: 21kDa

Comments:

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. Ras

a proto-oncogene

is a small G-protein that has 3 primary isoforms (H-Ras

N-Ras

and K-Ras) that differ in there approximately 20 C-terminal amino acids. H-Ras was first discovered as a transforming product the retrovirus Harvey murine virus and K-Ras of Kirten sarcoma virus. Ras is a heavily studied target of both academic and pharmaceutical research because of its implications in various pathways and diseases as well as being mutated in a large number of human cancers. Ras is most notably the activator of the Erk/MAPK kinase pathway as activator of Raf

as well as an activator of PI3 Kinase (PI3K). In its oncogenic

mutated state

Ras is unable to hydrolyze GTP to GDP

thus staying in an active state and activating numerous pathways including the MAPK pathway through its activation of Raf

but also others as well that include PI3 Kinase and RalGDS. One path that the pharmaceutical industry has taken to control Ras and its activity is by finding what some consider its Achilles’ heel. For its activation

Ras must localize to the plasma membrane

but interestingly

it lacks a transmembrane domain. To achieve this

Ras must first undergo a post-translational modification (PTM) known as prenylation or geranylation at its C-terminal CAAX motif. For this to take place

a controlled three step process must occur. The first step in the process is the prenylation or geranylation of the C in the CAAX motif that is initiated by the covalent attachment of farnesyl groups to the cysteine that is catalyzed by the . After this modification

the and heterodimer enzymes farnesyl transferases –aaX of the motif is proteolytically removed via Rce1 (Ras Converting Enzyme 1)

a membrane associated endoprotease

by a mechanism that is still not fully understood. Finally

the C-terminal prenylcysteine is now methlylated by ICMT (Isoprenylcysteine Carboxymethyl Transferase). These drugs have yet to pass clinical trials though and there is doubt that they will ever be successful in treating tumors associated with Ras activation.

Application Details

Application Notes: WB (1:100-500), ELISA (1:500-1000), IP (1:20-100), IHC-P (1:100-500), IHC-F (1:100-500), Flow-Cyt (1:20-100), IF (1:50-200)

Concentration: 1mg/1ml

Purification: affinity purified by Protein A

Buffer: 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide

Storage: Ship at room temperature. Store at -20°C

Restrictions: For Research Use only