Recombinant Human KRAS Protein (His Tag)

Name: Recombinant Human KRAS Protein (His Tag)
Brand: Beta LifeScience
SKU: BLPSN-3101
Availability: InStock

Collections: Enzymes, Other enzymes, Recombinant proteins

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Product Overview

Tag	His
Host Species	Human
Accession	AAH13572.1
Synonym	C-K-RAS, CFC2, K-RAS, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B, KI-RAS, KRAS1, KRAS2, NS, NS3, RALD, RASK2
Background	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 CheckpointImmunotherapyCancer ImmunotherapyTargeted Therapy
Description	A DNA sequence encoding the native human KRAS (AAH13572.1) (Thr 2-Cys 185) was expressed, with a His tag at the N-terminus.
Source	E.coli
Predicted N Terminal	Met
AA Sequence	Thr 2-Cys 185
Molecular Weight	The recombinant human KRAS consisting of 195 a.a. and has a calculated molecular mass of 22.5 kDa. It migrates as an 25 kDa band in SDS-PAGE under reducing conditions as predicted
Purity	>90% as determined by SDS-PAGE
Endotoxin	Please contact us for more information.
Bioactivity	Please contact us for detailed information
Formulation	Lyophilized from sterile 20mM Tris, 0.5M NaCl, pH 7.5.
Stability	The recombinant proteins are stable for up to 1 year from date of receipt at -70°C.
Usage	For Research Use Only
Storage	Store the protein under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Target Details

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.
Subcellular Location	Cell membrane; Lipid-anchor; Cytoplasmic side. Cytoplasm, cytosol.; [Isoform 2B]: Cell membrane; Lipid-anchor.
Protein Families	Small GTPase superfamily, Ras family
Database References	HGNC: 6407 OMIM: 190070 KEGG: hsa:3845 STRING: 9606.ENSP00000256078 UniGene: Hs.37003
Associated Diseases	Leukemia, acute myelogenous (AML); Leukemia, juvenile myelomonocytic (JMML); Noonan syndrome 3 (NS3); Gastric cancer (GASC); Cardiofaciocutaneous syndrome 2 (CFC2)

Gene Functions References

Pesticide exposure may play a great role in malignant transformation of urinary bladder cells through mutation in the K-ras gene. PMID: 29644616
deletion of the oncogenic KRAS allele resulted in enhanced STIM1 expression and greater Ca(2+) influx. PMID: 29748135
PIP5K1A loss reduces oncogenic KRAS signaling. PMID: 30194290
GATAD2B interacts with C-MYC to enhance KRAS driven tumor growth. PMID: 30013058
the present study demonstrates that miR-422a may serve as a tumor suppressor in osteosarcoma via inhibiting BCL2L2 and KRAS translation both in vitro and in vivo Therefore, miR-422a could be developed as a novel therapeutic target in osteosarcoma. PMID: 29358307
our studies demonstrate how KRAS inhibits the tumor suppressor RKIP, thus offering novel justification for targeting RKIP as a strategy to overcome KRAS-induced tumor metastasis and chemoresistance in PDAC. PMID: 29315556
This study confirms the tumor suppressor roles of miR-193a-3p, its downstream target affinity to KRAS and clinical significance in patients with colorectal adenocarcinoma. PMID: 29104111
in Stage I colorectal cancer presence of KRAS mutations, that of simultaneous mutations in PIK3CA gene, or that of multiple KRAS mutations was significantly associated with shorter cancer specific survival; PIK3CA or multiple KRAS mutations were associated with nodal micrometastases and poorly differentiated clusters G3 as well PMID: 30018674
Inhibition of Wee1 by its specific inhibitor MK1775 in combination with sorafenib restored the KRAS mutated cells' response to the multi-target tyrosine kinase inhibitor. PMID: 29343688
High FOS-like antigen 1 (FOSL1) expression with mutant KRAS protein lung and pancreatic cancer patients showed the worst survival outcome. PMID: 28220783
primary resistance to cetuximab is dependent upon both KRAS mutational status and protein expression level, and acquired resistance is often associated with KRAS(Q61) mutations that function even when protein expression is low. PMID: 28593995
The HSF1-BAG3-Mcl-1 signal axis is critical for protection of mutant KRAS colon cancer cells from AUY922-induced apoptosis. PMID: 29068469
Study results indicate that pleural homed cancer cells harboring activating KRAS mutations are competent of malignant pleural effusion induction. This genotype-phenotype link is primarily mediated via mutant KRAS-dependent CCL2 signaling that results in the recruitment of CD11b+Gr1+ myeloid cells to the pleural space. PMID: 28508873
Copy number gains were seen in EGFR (two of 23, 13.0%) and in one (4.3%) of each PIK3CA, KRAS, MET and STK11 PMID: 29489023
Study reveals the novel function of NOX4 in reprogramming aerobic glycolysis initiated by activated Kras and inactivated p16 in pancreatic ductal adenocarcinoma. PMID: 28232723
The role of KRAS oncogenic signaling in cancer cells.[review] PMID: 29263151
High KRAS expression is associated with Bladder Cancer. PMID: 29321082
Studies on the metabolic properties of mutant KRAS protein lung tumors have uncovered unique metabolic features that can potentially be exploited therapeutically [Review]. PMID: 28570035
Plasma membrane polyphosphoinositides depletion caused rapid translocation of K-Ras4B but not H-Ras from the plasma membrane to the Golgi. PMID: 28939768
we used hot-spot mutation sequencing to examine whether KRAS/NRAS mutations, a characteristic feature of mesonephric carcinoma,1 are also present in mesonephric hyperplasia. None of the mesonephric hyperplasia cases harboured a KRAS or NRAS mutation. PMID: 28703285
KRAS mutations are associated with colorectal liver metastases. PMID: 29937183
Our data provide evidence that blocking TfR could significantly inhibit lung adenocarcinoma (LAC) proliferation by targeting the oncogene KRAS; therefore, TfR may be a therapeutic target for LAC. In addition, our results suggest a new method for blocking the signal from the oncogene KRAS by targeting TfR in LAC. PMID: 29286585
Results show mutation in Kras was associated with worse survival results in patients with pancreatic neoplasm. [review] PMID: 30227250
CFTR exhibited an inhibitory role in the malignancy of lung adenocarcinoma A549 cells PMID: 29526175
characteristics of the expression of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), V-Ki-ras2 Kirsten rat sarcoma viral oncogene homologue (KRAS) in non-small cell lung cancer PMID: 30037374
Despite the presence of histological findings indicating long-standing gastroesophageal reflux in 25%, as well as symptomatic gastroesophageal reflux in more than 40%, there was no detectable tissue expression of KRAS or BRAF mutations in adult patients treated for esophageal atresia in childhood. PMID: 28873491
The high frequency of KRAS mutation in endometrial atypical hyperplasia with mucinous differentiation, endometrioid carcinoma with mucinous differentiation and mucinous carcinoma indicates that KRAS mutational activation is implicated in the pathogenesis of endometrial mucinous carcinoma. PMID: 30220122
The frequency of KRAS mutations was significantly higher in Serrated Lesions subgroups with low and intermediate methylated epigenotype tumors and microsatellite stability. PMID: 29974407
The rate of EGFR mutation was significantly higher in female and non-smoker patients. In TTF-1 positive cases EGFR mutation was more frequent. Age of the patients over 62-year old was correlated with KRAS mutations. The concordance between ALK IHC and FISH was 58.3%. The MET protein in the cases with MET amplification was 100% positive. PMID: 28756651
the findings demonstrated that mutated K-ras promotes cathepsin L expression and plays a pivotal role in EMT of human lung cancer. The regulatory effect of IR-induced cathepsin L on lung cancer invasion and migration was partially attributed to the Cathepsin L /CUX1-mediated EMT signaling pathway PMID: 29246726
These findings collectively suggest that the triple combination of survivin knockdown with ABT-263 and trametinib treatment, may be a potential strategy for the treatment of KRAS-mutant lung adenocarcinoma. Furthermore, our findings indicate that the welldifferentiated type of KRAS-mutant lung tumors depends, at least in part, on TTF1 for growth. PMID: 29658609
Increased long noncoding RNA HomeoboxA transcript at the distal tip (HOTTIP) expression was associated with poor prognosis independent of KRAS mutation. PMID: 29329159
Data show no patient positive for KRAS mutation and/or p53 mutation was found to have malignant transformation, suggesting detection of KRAS or p53 mutation in plasma is not an effective screening tool for pancreatic cancer because accumulation of multiple mutations is required for malignant transformation in the pancreas. PMID: 29303908
BCL-XL has a role in modulating RAS signalling to favor breast cancer cell stemness PMID: 29066722
KRAS is one of the most common mutations in Non-small cell lung cancer. [review] PMID: 29764594
Combination of PCR HRM with either RFLP or direct DNA sequencing was useful to detect K-RAS exon 2 and extended RAS mutations, respectively. Frequency of all RAS mutations in stage IV Indonesian (41%) was similar among Asians (41-49%), which tend to be lower than western (55%) CRC. PMID: 28044264
PPARgamma activator, pioglitazone, can activate p21, which is associated with decreased proliferation in 2 aerodigestive preneoplastic cell lines. In addition, the p21 gene may be a potential hypothesis-driven biomarker in translational studies of pioglitazone as a chemoprevention agent for aerodigestive cancer. PMID: 30047791
show that mutant KRAS facilitates IKKalpha-mediated responsiveness of tumor cells to host IL-1beta, thereby establishing a host-to-tumor signaling circuit that culminates in inflammatory MPE development and drug resistance PMID: 29445180
In a cohort of patients with pancreatic cysts, KRAS and GNAS mutations had no significant diagnostic benefit in comparison with conventional testing. PMID: 29796909
Results reveal that KRAS 3'UTR is a target for miR-19a which overexpression suppresses KRAS expression thus inhibiting angiogenesis in colorectal cancer. PMID: 29207158
observed that the trend is highly correlative of the rate of change in KRAS mutant DNA concentrations and the period of monitoring PMID: 28956302
Mutation frequencies in KRAS exon 3 or 4, NRAS, BRAF, and PIK3CA were 5.5%, 2.7%, 8.3%, and 5.5%, respectively. PMID: 29908105
Fluorescence cross-correlation data indicate no direct interaction between C6-ceramide and KRas4B, suggesting that KRas4B essentially recruits other lipids. A FRET-based binding assay reveals that the stability of KRas4B proteins inserted into the membrane containing C6-ceramide is reduced. PMID: 29357287
Identification of KRAS/NRAS/BRAF mutation status is crucial to predict the therapeutic effect and determine individual therapeutic strategies for patients with colorectal cancer. PMID: 29335867
KRAS mutation was significantly associated with tumor size PMID: 29103773
Our finding of frequent KRAS mutation in urachal adenocarcinoma suggests its potential role in the oncogenesis of this neoplasm PMID: 28285720
a low frequency of BRAF or KRAS mutation in Chinese patients with low-grade serous carcinoma of the ovary PMID: 29273082
The authors report that one of the K-Ras splice variants, K-Ras4a, is subject to lysine fatty acylation, a previously under-studied protein post-translational modification. Sirtuin 2 (SIRT2), one of the mammalian nicotinamide adenine dinucleotide (NAD)-dependent lysine deacylases, catalyzes the removal of fatty acylation from K-Ras4a. PMID: 29239724
Data indicate that absence of KRAS, TP53 and SMAD4 genetic alterations may identify a subset of pancreatic carcinomas with better outcome. PMID: 29103024
Proteoforms with or without the Gly13Asp mutation (G13D) in the KRAS4b isoform were studied in isogenic KRAS colorectal cancer (CRC) cell lines and patient CRC tumors with matching KRAS genotypes. In 2 cellular models, a direct link between knockout of the mutant G13D allele and complete nitrosylation of cysteine 118 of the remaining WT KRAS4b was observed. Major differences in C-terminal carboxymethylation were seen. PMID: 29610327

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