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Human KRAS (2-185, G12C) Protein, His Tag (active enzyme)

分子别名(Synonym)

GTPase Kras,K-Ras 2,Ki-Ras,c-K-ras,c-Ki-ras,KRAS2,RASK2,C-K-RAS,CFC2,K-RAS2A,K-RAS2B,K-RAS4A,K-RAS4B,KI-RAS,KRAS1,KRAS2,NS,NS3,RASK2,KRAS

表达区间及表达系统(Source)

Human KRAS (2-185, G12C) Protein, His Tag (KRS-H51H3) is expressed from E. coli cells. It contains AA Thr 2 - Cys 185 (Accession # P01116-2 (G12C)).

Predicted N-terminus: Met

Request for sequence

蛋白结构(Molecular Characterization)

KRAS Structure

This protein carries a polyhistidine tag at the N-terminus.

The protein has a calculated MW of 23.0 kDa. The protein migrates as 23-25 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE).

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>95% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in 20 mM Tris, 500 mM NaCl, pH7.5 with trehalose as protectant.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

KRAS SDS-PAGE

Human KRAS (2-185, G12C) Protein, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95% (With Star Ribbon Pre-stained Protein Marker).

 

活性(Bioactivity)

The specific activity of KRAS was determined to be> 400 pmol/min/mg in a GTPase-Glo assay using GTP solution substrate (QC tested).

Protocol

 
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背景(Background)

KRAS (Kirsten rat sarcoma 2 viral oncogene homolog) gene is a proto-oncogene that encodes a small GTPase transductor protein called KRAS. KRAS is also known as Ki-Ras, c-K-ras and
c-Ki-ras. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation, promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner. RAS is one of the most frequently mutated oncogenes in human cancer but the frequency and distribution of RAS gene mutations are not uniform. In details, mutation of glycine 12 (G12) causes RAS activation by interfering with GAP binding and GAP-stimulated GTP hydrolysis. The reference shows the pathway may as a potential therapy targets.

 

前沿进展

Enhancing KRAS G12D inhibitor sensitivity in pancreatic cancer through SHP2/PI3K pathway
Hao, Zhang, Dong et al
Med Oncol (2025) 42 (5), 139
Abstract: Pancreatic cancer with the KRAS G12D mutation, found in 40% of cases, is challenging to treat. MRTX1133, a non-covalent KRAS G12D inhibitor, shows therapeutic promise but faces resistance issues. Our study combines MRTX1133 with the SHP2 inhibitor SHP099 or PI3K inhibitor Buparlisib, showing synergistic inhibition of pancreatic cancer cell growth and enhanced apoptosis. These combination therapies could improve clinical outcomes for patients with KRAS G12D  mutation in pancreatic cancer.© 2025. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Antiproliferative and Apoptotic Efficacy of Nano-PLGA Encapsulated Quercetin Molecules by Downregulation of Akt in K-ras Mutated NSCLC Cell Lines, A549 and H460
Mukherjee, Ghosh, Ganguli et al
J Biochem Mol Toxicol (2025) 39 (4), e70240
Abstract: To test if encapsulating hydrophobic flavonoids in nanoparticles could offer a new possibility in the therapeutics of non-small cell lung cancer (NSCLC), quercetin was encapsulated in Poly(lactic-co-glycolic acid) (PLGA) nanoparticles by the solvent displacement technique. The synthesized nanoparticles were then characterized by dynamic light scattering (DLS), Fourier transform infrared spectroscopy (FTIR), and atomic force microscopy (AFM). The size of the nanoparticles with smooth surface topology was estimated at 110 nm. Treatment with nano-PLGA encapsulated quercetin (NPEQ) triggered the death of K-ras mutated NSCLC cells, A549 and H460, and showed 50% cell cytotoxicity in them at a dose of 406 and 347 ng/ml respectively. NPEQ was able to block uncontrolled cell proliferation by inducing concomitant destruction of BrdU activity and a lower incidence of cell migrations. Cell death was due to the induction of apoptosis rather than necrosis, as revealed by morphological alterations and phosphatidylserine externalization induced by NPEQ. NPEQ also caused the arrest of A549 and H460 cells at the sub-G1 stage. Through network analysis, AKT was identified as a key gene target of quercetin in NSCLC. Moreover, we found that NPEQ induced downregulation of Akt, which is usually hyperactive in NSCLC due to K-ras mutation. This indicates that NPEQ caused target-specific apoptotic and antiproliferative activity by targeting the downregulation of Akt. Further, when NPEQ was generated in the tumour-bearing mice model, it showed antitumor efficacy also modulating the Akt expression along with upregulation in cleaved caspase 3 activation. Besides this, histological alteration of tissue architecture and reduction in tumor volume was also found. This as a whole indicates the prospects and advantages of nanoparticulate quercetin delivery in therapeutic formulations against cancer.© 2025 Wiley Periodicals LLC.
A Narrative Review of RAS Mutations in Early-Stage Colorectal Cancer: Mechanisms and Clinical Implications
Yildirim, Gunenc, Almuradova et al
Medicina (Kaunas) (2025) 61 (3)
Abstract: Colorectal cancer (CRC) is the third-most common cancer globally and a leading cause of cancer-related deaths. While the prognostic and predictive roles of RAS mutations in advanced CRC are well-established, their significance in early-stage CRC remains a topic of debate. Studies have been conducted for many years on clinical and pathological parameters that may be associated with RAS mutation, and there are inconsistent results in this regard. Currently, the only biomarker used in early-stage CRC is microsatellite status. KRAS mutations are detected in 40-50% of patients with colorectal cancer. RAS activating mutations cause loss of EGFR regulation by acting on the RAS/RAF/MAPK signaling pathways. In advanced colorectal cancer, these mechanisms cause a decrease in the effectiveness of EGFR inhibitors. However, studies on patients with early-stage colorectal cancer have inconsistent results. This review highlights the prognostic and clinical significance of KRAS mutations in early-stage CRC, particularly in MSS tumors. In the MSS group, KRAS mutations were associated with shorter TTR and OS compared to DWT patients. In contrast, in the MSI-H group, KRAS mutations showed no prognostic effect in TTR and OS. However. KRAS mutations were associated with shorter SAR in both MSI-H and MSS groups of patients. The findings underscore the need for routine molecular profiling, including KRAS and MSI status, to refine risk stratification and guide adjuvant therapy decisions. Further studies are warranted to explore targeted therapeutic approaches for KRAS-mutant CRC in the adjuvant setting.
KRAS-SOS-1 Inhibition as New Pharmacological Target to Counteract Anaplastic Thyroid Carcinoma (ATC)
Mannino, Basilotta, De Luca et al
Int J Mol Sci (2025) 26 (6)
Abstract: Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer. Tumor cells have been shown to activate alternative signaling pathways, making treatments less effective. One of the major proteins involved in the progression of ATC is the proto-oncogene KRAS that belongs to a group of small guanosine triphosphate (GTP)-binding proteins. Despite its recognized importance in cancer malignancy, KRAS is considered non-druggable and has never been studied in the field of ATC. In this context, a new synthetic molecule, BAY-293, has recently been developed that selectively inhibits the KRAS-SOS-1 interaction. Based on these findings, the aim of this study was to evaluate for the first time the antitumor effect of BAY-293 using in vitro and in vivo models of ATC. The in vitro model included different thyroid cancer (TC) cell lines used to study the effect of BAY-293 on the modulation of mitogen-activated protein kinase (MAPK) pathways, apoptosis, and cell migration. To confirm the in vitro findings and better mimic the complex tumor microenvironment, an in vivo orthotopic model of ATC was used. The results of the study indicate that BAY-293, both in vitro and in vivo, effectively blocked the KRAS/MAPK/ERK pathway and β-catenin, which act as downstream effectors essential for cell migration, and increased the apoptotic process by slowing the progression of ATC. In conclusion, this study demonstrated that KRAS/SOS-1 inhibition could be a promising therapeutic target for the treatment of ATC and highlighted BAY-293 as an innovative molecule that needs further research to fully evaluate its efficacy in the field of thyroid cancer.
Showing 1-4 of 28964 papers.
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KRAS靶点信息
英文全称:GTPase KRas
中文全称:V-Ki-ras2 Kirsten大鼠肉瘤病毒癌基因同源蛋白
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:29详情
最高研发阶段:临床二期
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