Recombinant Human GTPase KRas(KRAS),partial

Code CSB-EP012493HU1
Size $1726
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Purity Greater than 90% as determined by SDS-PAGE.
Target Names KRAS
Uniprot No. P01116
Research Area Epigenetics and Nuclear Signaling
Alternative Names 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
Species Homo sapiens (Human)
Source E.coli
Expression Region 2-168aa
Target Protein Sequence TEYKLVVVGAGGVGKSALTIQLIQNHFVDEYDPTIEDSYRKQVVIDGETCLLDILDTAGQEEYSAMRDQYMRTGEGFLCVFAINNTKSFEDIHHYREQIKRVKDSEDVPMVLVGNKCDLPSRTVDTKQAQDLARSYGIPFIETSAKTRQRVEDAFYTLVREIRQYRL
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight 23.1kDa
Protein Length Partial
Tag Info N-terminal 6xHis-tagged
Form Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Troubleshooting
and FAQs
Protein FAQs
Storage Condition Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA Please contact us to get it.

Target Data

Function Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation
Gene References into Functions
  1. Pesticide exposure may play a great role in malignant transformation of urinary bladder cells through mutation in the K-ras gene. PMID: 29644616
  2. deletion of the oncogenic KRAS allele resulted in enhanced STIM1 expression and greater Ca(2+) influx. PMID: 29748135
  3. PIP5K1A loss reduces oncogenic KRAS signaling. PMID: 30194290
  4. GATAD2B interacts with C-MYC to enhance KRAS driven tumor growth. PMID: 30013058
  5. 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
  6. 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
  7. 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
  8. 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
  9. 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
  10. High FOS-like antigen 1 (FOSL1) expression with mutant KRAS protein lung and pancreatic cancer patients showed the worst survival outcome. PMID: 28220783
  11. 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
  12. The HSF1-BAG3-Mcl-1 signal axis is critical for protection of mutant KRAS colon cancer cells from AUY922-induced apoptosis. PMID: 29068469
  13. 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
  14. 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
  15. Study reveals the novel function of NOX4 in reprogramming aerobic glycolysis initiated by activated Kras and inactivated p16 in pancreatic ductal adenocarcinoma. PMID: 28232723
  16. The role of KRAS oncogenic signaling in cancer cells.[review] PMID: 29263151
  17. High KRAS expression is associated with Bladder Cancer. PMID: 29321082
  18. 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
  19. Plasma membrane polyphosphoinositides depletion caused rapid translocation of K-Ras4B but not H-Ras from the plasma membrane to the Golgi. PMID: 28939768
  20. 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
  21. KRAS mutations are associated with colorectal liver metastases. PMID: 29937183
  22. 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
  23. Results show mutation in Kras was associated with worse survival results in patients with pancreatic neoplasm. [review] PMID: 30227250
  24. CFTR exhibited an inhibitory role in the malignancy of lung adenocarcinoma A549 cells PMID: 29526175
  25. 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
  26. 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
  27. 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
  28. The frequency of KRAS mutations was significantly higher in Serrated Lesions subgroups with low and intermediate methylated epigenotype tumors and microsatellite stability. PMID: 29974407
  29. 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
  30. 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
  31. 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
  32. Increased long noncoding RNA HomeoboxA transcript at the distal tip (HOTTIP) expression was associated with poor prognosis independent of KRAS mutation. PMID: 29329159
  33. 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
  34. BCL-XL has a role in modulating RAS signalling to favor breast cancer cell stemness PMID: 29066722
  35. KRAS is one of the most common mutations in Non-small cell lung cancer. [review] PMID: 29764594
  36. 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
  37. 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
  38. 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
  39. In a cohort of patients with pancreatic cysts, KRAS and GNAS mutations had no significant diagnostic benefit in comparison with conventional testing. PMID: 29796909
  40. 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
  41. observed that the trend is highly correlative of the rate of change in KRAS mutant DNA concentrations and the period of monitoring PMID: 28956302
  42. 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
  43. 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
  44. 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
  45. KRAS mutation was significantly associated with tumor size PMID: 29103773
  46. Our finding of frequent KRAS mutation in urachal adenocarcinoma suggests its potential role in the oncogenesis of this neoplasm PMID: 28285720
  47. a low frequency of BRAF or KRAS mutation in Chinese patients with low-grade serous carcinoma of the ovary PMID: 29273082
  48. 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
  49. Data indicate that absence of KRAS, TP53 and SMAD4 genetic alterations may identify a subset of pancreatic carcinomas with better outcome. PMID: 29103024
  50. 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
  51. GNAS mutation is a highly specific test for IPMN. When GNAS testing is added to CEA and KRAS, a significantly greater overall accuracy (86.2%) is achieved. PMID: 27514845
  52. Knowing the mutation status of KRAS, BRAF or PIK3CA in stage II colorectal cancer can significantly improve the accuracy of prognoses. PMID: 28685592
  53. KRAS mutations were predominant in non-Squamous cell carcinomas of the cervix and were associated with HPV 18 infection. A combination of KRAS mutation detection and HPV genotyping would be useful in identifying patient with poor prognosis for further interventions. PMID: 29185262
  54. Of 106 KRAS protein (KRAS) mutations detected in 171 pancreatic juice samples, 58 were detected in the 5-minute samples, 70 mutations were detected in the 10-minute samples, and 65 were detected in the 15-minute samples. PMID: 29200129
  55. Results showed that KRAS was upregulated in melanoma tissues and inversely correlated with miR-326 expression and that miR-326 could directly target its 3'-UTR. In addition, the KRAS knockdown phenocopied the tumor-suppressing effects of miR-326 overexpression on melanoma cells. The restoration of the expression of KRAS markedly reversed the antitumor effects induced by miR-326 overexpression in melanoma cells. PMID: 29115540
  56. We have investigated if the initial source of intratumoral heterogeneity is consequent to multiple independent lineages derived from different crypts harboring distinct truncal APC and driver KRAS mutations, thus challenging the prevailing monoclonal monocryptal model. PMID: 28645942
  57. KRAS mutations were only associated with risk of death. PMID: 29223986
  58. we have found that a subgroup of colorectal cancers, defined by having either KRAS or BRAF (KRAS/BRAF) mutations and BCL2L1 (encoding BCL-XL) amplification, can be effectively targeted by simultaneous inhibition of BCL-XL (with ABT-263) and MCL1 (with YM-155). PMID: 28611106
  59. the resveratrol derivative did not affect the growth of HKe3 cell spheroids derived from HCT116 cells by disruption of the activating mutant KRAS gene. These results suggest that the resveratrol derivative inhibits the growth of HCT116 cell spheroids via inhibition of an oncogenic KRAS-mediated signaling pathway. PMID: 28936721
  60. Kras regulates circular RNA in colon cancer cells. PMID: 27892494
  61. these results suggest that aspirin inhibited human uterine leiomyoma cell growth by regulating KRasp110alpha interaction. Aspirin which targeting on interaction between K-Ras and p110alpha may serve as a new therapeutic drug for uterine leiomyoma treatment. PMID: 28849118
  62. These results suggested that miR337 may act as a tumour suppressor during the process of CRC malignant transformation by interacting with KRAS PMID: 29048669
  63. These data reveal previously unknown genomic diversity among KrasG12D-initiated GEMM tumors, places them in context of human patients, and demonstrates how to exploit this inherent tumor heterogeneity to discover therapeutic vulnerabilities. PMID: 29203670
  64. Digital droplet PCR reliably detects KRAS G12D mutations in stool-derived DNA from colorectal cancer patients, especially at early stages. PMID: 29093617
  65. results thus provide the first detailed insight into the multiplicity, structure, and membrane organization of K-Ras homomers PMID: 28863262
  66. Programmed cell death 1 ligand 1 protein (PD-L1) expression significantly correlates with overall mutational load and KRAS protein mutational status in pulmonary sarcomatoid carcinomas. PMID: 29110857
  67. Our findings showed BRAF and/or KRAS mutations in three of seven cases of low-grade serous neoplasms of the testis PMID: 28543997
  68. Intratumoral heterogeneity of the KRAS mutational status is rare in pancreatic ductal adenocarcinoma. In addition, no KRAS heterogeneity between primary tumors and metastatic lymph nodes was detected in this study. PMID: 26967456
  69. ALK and KRAS mutations are associated with acquired resistance to crizotinib in ALK-positive non-small cell lung cancer PMID: 28601386
  70. Altogether, these data show that humanized anti-progastrin antibodies might represent a potential new treatment for K-RAS-mutated colorectal patients, for which there is a crucial unmet medical need PMID: 28600477
  71. longitudinal monitoring of urine specimens showed an increase in the quantity of mutant KRAS transrenal DNA, which were highly associated with disease progression and outcome. PMID: 27998182
  72. The presence of KRAS mutations did not enrich for the activation of IL-6, JAK1 or phosphorylated STAT3 in resected lung adenocarcinoma. PMID: 28879441
  73. Due to the discordant results (GGT->GTT exon 2 KRAS mutation in the primary tumor, and KRAS-WT in the liver metastases), mutational analysis on liver metastasis was repeated using next-generation sequencing and enriching the sample in tumor cells by manual microdissection; the same type of mutation of the primary tumor (GGT->GTT exon 2 KRAS gene) was confirmed PMID: 28665451
  74. KRAS mutations appear to be major driver genetic alterations in both liver and pancreatic mucinous cystic neoplasms (MCNs). PMID: 28570009
  75. Circulating tumor DNA may serve as a viable alternative to tissue analysis for the detection of KRAS mutations in colorectal cancer PMID: 28885658
  76. Collection of transrenal DNA, being noninvasive, is an attractive assay and easily allows serial monitoring of the disease. Results from preoperative detection showed a close correlation to tumor tissue profiling and demonstrated close associations to the disease. We also observed significant decreases in mutant KRAS DNA concentration after surgery, which confirmed transrenal DNA's sensitivity to treatment response. PMID: 28708207
  77. Expression of Ki-67, p53 and K-ras in the intestinal mucosa was detected by immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. 1.03% patients (n = 7) underwent polypectomy was confirmed to be the early stage of Colorectal cancer (CRC). Histological analysis for expression of p53 and K-ras can guarantee to screen the early stage of CRC. PMID: 29104470
  78. Deciphering KRAS and NRAS mutated clone dynamics in MLL-AF4 paediatric leukaemia by ultra deep sequencing analysis. PMID: 27698462
  79. these results describe a novel mechanism governing PRKD1 gene expression in pancreatic ductal adenocarcinoma and provide a functional link between oncogenic KRas, NF-kappaB and expression of PRKD1. PMID: 27649783
  80. Data suggest that the co-existence of KRAS mutations and high MYC expression predicts anti-mitotic drug sensitivity. PMID: 27412232
  81. activated Ras, protumorigenic COX-2 and Notch1 have roles in in papillary mucinous neoplasm onset PMID: 27381829
  82. while telomere length did not correlate with the presence of a mutation in BRAF (V-raf murine sarcoma viral oncogene homolog B), PIK3CA (phosphatidylinositol 3-kinase catalytic subunit), or MSI status, it was significantly associated with the occurrence of a mutation in KRAS PMID: 28850092
  83. Exposure to cetuximab and various concentration of AG490, an inhibitor of JAK2, STAT3 and HSP27 protein levels, except in the KRAS G12V mutant line, SW620...cetuximab may promote SN38 sensitivity via suppression of HSP27, through blocking the JAK/STAT signaling pathway, and shows synergistic effects when combined with SN38 in wild-type RAS CRC cells. PMID: 28656305
  84. In this study we report a new delivery strategy for a G4-decoy oligonucleotide that sequesters MAZ, a transcription factor essential for KRAS transcription. It is based on the use of palmitoyl-oleyl-phosphatidylcholine (POPC) liposomes functionalized with lipid-modified G4-decoy oligonucleotides and a lipid-modified cell penetrating TAT peptide PMID: 27929127
  85. Our up-to-date review discusses CaM's role in PI3K signaling at the membrane in KRAS-driven cancers. This is significant since it may help development of K-Ras-specific pharmacology. PMID: 28462395
  86. These findings suggest that future trials of everolimus in biliary tract cancer would benefit from preselecting patients based on their K-Ras and PI3K/mTOR pathway activation status. PMID: 28544747
  87. we detected mutually exclusive KRAS and MAP2K1 mutations in one-third of cases of Rosai-Dorfman disease PMID: 28664935
  88. Human and mouse studies reveal that different gene dosages of an activating KRAS mutation are critical determinants of pancreatic cancer biology, including early progression, metastasis, histopathology, cellular plasticity and clinical aggressiveness. PMID: 29364867
  89. Our results demonstrated increased expression of both K-Ras mRNA splicing variants in leiomyoma tissue. However, the ultimate result of KRAS expression on leiomyoma development depends on the overall KRAS isoform balance and, consequently, on activated signaling pathways. PMID: 28122482
  90. observations add to a body of evidence suggesting that HRAS and KRAS show meaningful differences in functionality stemming from differential protein dynamics independent of the hypervariable region PMID: 29235861
  91. KRAS and BRAF mutations are negatively associated with overall and relapse-free survival in patients who undergo complete liver resection for colorectal cancer liver metastases PMID: 28216246
  92. study is the first to identify driver-follower relationships in correlated motions of K-Ras residue pairs, revealing the direction of information flow during allosteric modulation of its nucleotide-dependent intrinsic activity: active K-Ras Switch-II region motions drive Switch-I region motions, while alpha-helix-3L7 motions control both. PMID: 27845397
  93. The high incidence of KRAS mutations in papillary mucinous metaplasia suggests that papillary mucinous metaplasia may be a precancerous lesion of a certain subset of mucinous carcinomas of the endometrium PMID: 29715099
  94. The present case series suggests that the incidence of concomitant KRAS/BRAF mutations in patients with surgically treated colorectal liver metastasis may be higher than previously hypothesized, and associated with more variable survival outcomes than expected. PMID: 29715113
  95. in vitro results showed that the repression of KRAS by miR-16 suppressed the proliferation and invasion and induced the apoptosis of colorectal cancer (CRC) cells, and the in vivo results revealed that miR-16 exerted a tumor-suppressive effect by negatively regulating KRAS in xenograft mice. Taken together, our findings provide evidence supporting the role of miR-16 as a tumor suppressor in CRC by targeting KRAS PMID: 27857191
  96. k-RAS gene mutation status was associated with the response of Gefitinib treatment in patients with nonsmall-cell lung cancer PMID: 28901317
  97. we demonstrate that oncogenic p110alphaH1047R, K-RasG12V, H-RasG12V, and Her2 use a common Akt1-FOXO3a pathway in suppression of DeltaNp63alpha expression and, consequently, promote cell migration/invasion and tumor metastasis. Thus, DeltaNp63alpha may function as a critical integrator of oncogenic signals in cell motility and cancer metastasis. PMID: 28468801
  98. In the colorectal biopsies from 50 patients with suspected colorectal cancer, 18 cases (36%) contained mutant KRAS, and the amount of mutant DNA accounted for 18.664.2% of the total DNA. PMID: 28677778
  99. KRAS mutation patterns in Sri Lankan metastatic colorectal cancer: p.Gly13Asp (40.0%), p.Gly12Val (24.0%),p.Gly12Cys (12.0%), p.Gly12Ser (12.0%), p.Gly12Asp (8.0%), and p.Gly12Arg (4.0%). The codon 13 mutation was a G>A transition (40.0%), while G>T transversions (32.0%), G>A transitions (24.0%), and G>C transversions (4.0%) were found in the codon 12 mutations. PMID: 28797274
  100. It is unclear if we may have seen greater clinical activity if we were able to fully inhibit Src in this study, but given the requirement that enrolling patients have documented disease progression on cetuximab, acquired resistant KRAS-mutant clones may have been present, limiting future strategies to reverse EGFR resistance PMID: 28280091

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Involvement in disease Leukemia, acute myelogenous (AML); Leukemia, juvenile myelomonocytic (JMML); Noonan syndrome 3 (NS3); Gastric cancer (GASC); Cardiofaciocutaneous syndrome 2 (CFC2)
Subcellular Location Cell membrane, Lipid-anchor, Cytoplasmic side, Cytoplasm, cytosol
Protein Families Small GTPase superfamily, Ras family
Database Links

HGNC: 6407

OMIM: 190070

KEGG: hsa:3845

STRING: 9606.ENSP00000256078

UniGene: Hs.37003

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