KRAS cDNA ORF Clone in Cloning Vector, Human

Cat: HG12259-G

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KRAS cDNA ORF Clone in Cloning Vector, Human General Information

Gene

Species
Human
NCBI Ref Seq
RefSeq ORF Size
567 bp
Sequence Description
Identical with the Gene Bank Ref. ID sequence.
Description
Full length Clone DNA of Human v-Ki-ras2 Kirsten rat sarcoma viral oncogene homol.

Plasmid

Vector
Sequencing Primers
SP6 and T7 or M13-47 and RV-M
Quality Control
The plasmid is confirmed by full-length sequencing.

Screening

Antibiotic in E.coli
Ampicillin

Storage & Shipping

Shipping
Each tube contains lyophilized plasmid.
Storage
The lyophilized plasmid can be stored at ambient temperature for three months.

KRAS cDNA ORF Neucleotide Sequence and Amino Acid Sequence Information

**Sino Biological guarantees 100% sequence accuracy of all synthetic DNA constructs we deliver, but we do not guarantee protein expression in your experimental system. Protein expression is influenced by many factors that may vary between experiments or laboratories.**

KRAS cDNA ORF Clone in Cloning Vector, Human Alternative Names

C-K-RAS cDNA ORF Clone, Human;CFC2 cDNA ORF Clone, Human;K-RAS cDNA ORF Clone, Human;K-RAS2A cDNA ORF Clone, Human;K-RAS2B cDNA ORF Clone, Human;K-RAS4A cDNA ORF Clone, Human;K-RAS4B cDNA ORF Clone, Human;KI-RAS cDNA ORF Clone, Human;KRAS1 cDNA ORF Clone, Human;KRAS2 cDNA ORF Clone, Human;NS cDNA ORF Clone, Human;NS3 cDNA ORF Clone, Human;RALD cDNA ORF Clone, Human;RASK2 cDNA ORF Clone, Human

KRAS Background Information

K-Ras belongs to the small GTPase superfamily, Ras family. As other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity which cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example RasGAP. In turn K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations have been found to be associated with Noonan syndrome[4] and cardio-facio-cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer and lung cancer.

Immune Checkpoint   Immunotherapy   Cancer Immunotherapy   Targeted Therapy

Full Name
Kirsten rat sarcoma viral oncogene homolog
References
  • Ling J, et al. (2012) KrasG12D-induced IKK2//NF-B activation by IL-1 alpha and p62 feedforward loops is required for development of pancreatic ductal adenocarcinoma. Cancer Cell. 21(1):105-20.
  • Matallanas D, et al. (2011) Mutant K-Ras activation of the proapoptotic MST2 pathway is antagonized by wild-type K-Ras. Mol Cell. 44(6):893-906.
  • Regala RP, et al. (2011) Matrix metalloproteinase-10 promotes Kras-mediated bronchio-alveolar stem cell expansion and lung cancer formation. PLoS One. 6(10):e26439.
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