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The Human KRAS recombinant protein is conventionally generated by transfecting the recombinant DNA into a host cell, and then the host cells are cultured and the transfected DNA transcribed and translated. Different host cells can be chosen for recombinant protein production, the choice of which depends on the type of protein that needs to be generated, its functional activity and requisite yield. We choose E.coli?as the expression system for this KRAS protein expression because bacteria cells are easy to culture, grow fast and produce high yields of recombinant protein.KRAS is a protein coding gene that encodes GTPase KRas. According to some research, KRAS may have the following features.KRAS mutation status predicts colorectal cancer response to cetuximab therapy. KRAS proteins play an important role in human cancers but have not yet succumbed to therapeutic attack. By determining the mutational status of EGFR and KRAS, treatment decisions regarding the use of these kinase inhibitors may be improved. GTPase KRAS inhibits the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells. The quantitative biophysical analysis identified key components that regulate the recruitment of the GTPase KRAS to the plasma membrane.
The Human KRAS recombinant protein is conventionally generated by transfecting the recombinant DNA into a host cell, and then the host cells are cultured and the transfected DNA transcribed and translated. Different host cells can be chosen for recombinant protein production, the choice of which depends on the type of protein that needs to be generated, its functional activity and requisite yield. We choose E.coli?as the expression system for this KRAS protein expression because bacteria cells are easy to culture, grow fast and produce high yields of recombinant protein.KRAS is a protein coding gene that encodes GTPase KRas. According to some research, KRAS may have the following features.KRAS mutation status predicts colorectal cancer response to cetuximab therapy. KRAS proteins play an important role in human cancers but have not yet succumbed to therapeutic attack. By determining the mutational status of EGFR and KRAS, treatment decisions regarding the use of these kinase inhibitors may be improved. GTPase KRAS inhibits the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells. The quantitative biophysical analysis identified key components that regulate the recruitment of the GTPase KRAS to the plasma membrane.
| Cat.No | ACP05083 | Target Name | KRAS |
|---|---|---|---|
| Form | Liquid or Lyophilized powder | Expression System | E.coli |
| Expression Range | 2-168aa | Mol Weight | 23.1kDa |
| Protein Length | Partial | Purity | Greater than 90% as determined by SDS-PAGE. |
| Storage Buffer | 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0. |
| Target Species | Human | Uniprot ID | P01116 |
|---|
Uniprot Id
P01116
Target Species
Human
Target Name
KRAS
Target Full Name
GTPase KRas
Target Function
Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation. 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.
Target Involvement
Leukemia, acute myelogenous (AML); Leukemia, juvenile myelomonocytic (JMML); Noonan syndrome 3 (NS3); Gastric cancer (GASC); Cardiofaciocutaneous syndrome 2 (CFC2)
Target Subcellular Location
Cell membrane; Lipid-anchor; Cytoplasmic side. Cytoplasm, cytosol.; [Isoform 2B]: Cell membrane; Lipid-anchor.
Target Protein Families
Small GTPase superfamily, Ras family
Target Research Area
Epigenetics and Nuclear Signaling
Target Synonyms
c Ki ras2; c Kirsten ras protein; c-K-ras; c-Ki-ras; Cellular c Ki ras2 proto oncogene; Cellular transforming proto oncogene; CFC2; cK Ras; GTPase KRas; K RAS p21 protein; K RAS2A; K RAS2B; K RAS4A; K RAS4B; K-Ras 2; KI RAS; Ki-Ras; KIRSTEN MURINE SARCOMA VIRUS 2; Kirsten rat sarcoma 2 viral (v Ki ras2) oncogene homolog; Kirsten rat sarcoma viral oncogene homolog; KRAS; KRAS proto oncogene, GTPase; KRAS1; KRAS2; N-terminally processed; NS; NS3; Oncogene KRAS2; p21ras; PR310 c K ras oncogene; PR310 cK ras oncogene; RALD; RASK_HUMAN; RASK2; Transforming protein p21; v Ki ras2 Kirsten rat sarcoma 2 viral oncogene homolog; v Ki ras2 Kirsten rat sarcoma viral oncogene homolog
Target 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.
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