登录 | 注册    关注公众号  
微信公众号
搜索
 >  Protein>KRAS >KRS-H51H5

Human KRAS (Q61H) 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 (Q61H), His Tag (KRS-H51H5) is expressed from E. coli cells. It contains AA Thr 2 - Cys 185(Q61H) (Accession # P01116-2 (Q61H)).

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 26-27 kDa under reducing (R) condition (SDS-PAGE).

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in 50 mM Tris, 0.5 M 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 (Q61H), His Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90%.

 

活性(Bioactivity)

The specific activity of KRAS was determined to be > 350 pmol/min/mg in a GTPase-Glo assay using GTP solution substrate (QC tested).

Protocol

 
评论(0)
  1. 177XXXXXXX7
  2. 0人赞
  3. 人源CD172a抗原,带HIS标签,octect仪器使用proA传感器结合抗原,检测抗体抗原结合强弱,筛选抗体。
  4. >
  5. 2021-11-10
  1. 136XXXXXXX5
  2. 0人赞
  3. 该产品主要用于对比分析,应用于Elisa结合活性实验,最后得到的结果还是比较满意的,对照组也无非特异性结合!蛋白也比较稳定!
  4. 2021-8-19
  1. 166XXXXXXX7
  2. 0人赞
  3. 人源SIPR a V2/CD172a抗原,带HIS标签,通过在FAB端结合抗原,通过proA传感器结合抗原,检测抗体抗原结合强弱,筛选抗体。
  4. 2021-9-30
 
ACRO质量管理体系
 
 

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

KRAS G12V mutation-selective requirement for ACSS2 in colorectal adenoma formation
Budagyan, Cannon, Chatoff et al
Cell Rep (2025) 44 (4), 115444
Abstract: Oncogenic KRAS mutations are prevalent in colorectal cancer (CRC) and linked to poor prognosis and therapeutic resistance. Emerging evidence suggests that specific KRAS mutations differentially influence treatment responses. In this study, we generate isogenic Apc-null mouse colon epithelial cells with four common KRAS mutations. Transcriptomic and proteomic analyses reveal significant enrichment of cholesterol and lipid metabolism pathways in KRAS G12V cells, driven by increased SREBP1 expression and mTORC1 activation. Furthermore, KRAS G12V cells exhibit elevated ACSS2 expression and greater dependence on ACSS2 for proliferative advantage compared to other mutants. Inhibition of ACSS2 uniquely sensitizes KRAS G12V cells to MEK inhibition, highlighting a distinct therapeutic vulnerability. Finally, ACSS2 plays a critical role in early KRAS G12V adenoma development, unlike in KRAS G12D adenomas. These findings highlight mutation-specific metabolic reprogramming in KRAS-driven CRC and identify ACSS2 as a potential therapeutic target.Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.
Local DIO2 Elevation Is an Adaption in Malformed Cerebrovasculature
Li, Tang, Wang et al
Circ Res (2025)
Abstract: Cerebrovascular malformations are a pivotal cause of hemorrhage and neurological disability alongside lacking effective medication. Thyroid hormones (THs), including thyroxine and triiodothyronine, are essential for vascular development, yet whether they participate in malformed cerebrovascular pathology remains elusive.Single-cell transcriptome analysis characterized human cerebral cavernous malformations and brain arteriovenous malformations, 2 typical cerebrovascular malformation diseases. Adeno-associated virus-mediated DIO2 (iodothyronine deiodinase 2; an enzyme that converts thyroxine to active triiodothyronine) overexpression/knockdown or triiodothyronine/methimazole (an antithyroid drug) treatment was applied to mouse models of cerebral cavernous malformations (endothelial-specific Pdcd10 knockout mice, Pdcd10 KO) and brain arteriovenous malformations (endothelial-specific KrasG12D mutant mice, KrasG12D) to evaluate the involvement of DIO2 and TH signaling in cerebrovascular malformations.TH signaling was markedly activated in fibroblasts of human cerebral cavernous malformation and arteriovenous malformation single-cell samples, accompanied by elevated DIO2 expression. Similar DIO2 upregulation was observed in cerebrovascular fibroblasts of Pdcd10 KO/KrasG12D mice and patient brain sections. Exogenous DIO2 or triiodothyronine replenishment effectively reduced brain hemorrhage, excessive ECM (extracellular matrix) remodeling, and vascular leakage in juvenile and adult male and female Pdcd10 KO/KrasG12D mice. In contrast, DIO2 silencing or TH inhibition deteriorated vascular anomalies. Mechanistically, transcription factor Foxk1 (forkhead box K1) was determined to interact with the DIO2 promoter region. The activation of fibroblast PI3K-Akt-mTOR signaling in Pdcd10 KO/KrasG12D mice triggered Foxk1 nuclear translocation to promote DIO2 transcription. Triiodothyronine treatment mitigated inflammatory infiltration, normalized mitochondrial morphology, and restored mitochondrial biogenesis in malformed brain vessels by activating the Pgc1a (peroxisome proliferator-activated receptor gamma coactivator 1-alpha)-Sod2 (superoxide dismutase 2)/Prdx3 (peroxiredoxin 3)/Gpx1 (glutathione peroxidase 1) axis to reduce reactive oxygen species accumulation. We also determined that the vascular repair effects of triiodothyronine were Pgc1a-dependent.We delineate a novel DIO2-mediated adaption in malformed cerebrovasculature and conclude that targeting TH signaling may represent a potential therapy for cerebrovascular disorders.
Editorial: KRAS in stage IV non-small cell lung cancer
Noordhof, Blum, Hardavella et al
Front Oncol (2024) 14, 1517049
Showing 1-4 of 28946 papers.
Powered by BizGenius
 
 
货号/价格
文档
联系电话:
+86 400-682-2521(全国)
010-53681107(北京)
021-50850665(上海)
运输方式
订单邮箱:
order.cn@acrobiosystems.com
技术支持邮箱:
tech.cn@acrobiosystems.com
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
查看更多信息
前沿进展
点击查看详细
相关产品
View All KRAS

消息提示

请输入您的联系方式,再点击提交!

确定