Human GTPase KRas(KRAS) ELISA kit

Code CSB-EL012493HU
Size 96T,5×96T,10×96T
Price Request a Quote or Start an on-line Chat
Trial Size 24T ELISA Kit Trial Size (Only USD$150/ kit)
* The sample kit cost can be deducted from your subsequent orders of 96T full size kits of the same analyte at 1/5 per kit, until depleted in 6 months. Apply now

Product Details

Target Name
v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog
Alternative Names
c Ki ras2 ELISA Kit; c Kirsten ras protein ELISA Kit; c-K-ras ELISA Kit; c-Ki-ras ELISA Kit; Cellular c Ki ras2 proto oncogene ELISA Kit; Cellular transforming proto oncogene ELISA Kit; CFC2 ELISA Kit; cK Ras ELISA Kit; GTPase KRas ELISA Kit; K RAS p21 protein ELISA Kit; K RAS2A ELISA Kit; K RAS2B ELISA Kit; K RAS4A ELISA Kit; K RAS4B ELISA Kit; K-Ras 2 ELISA Kit; KI RAS ELISA Kit; Ki-Ras ELISA Kit; KIRSTEN MURINE SARCOMA VIRUS 2 ELISA Kit; Kirsten rat sarcoma 2 viral (v Ki ras2) oncogene homolog ELISA Kit; Kirsten rat sarcoma viral oncogene homolog ELISA Kit; KRAS ELISA Kit; KRAS proto oncogene, GTPase ELISA Kit; KRAS1 ELISA Kit; KRAS2 ELISA Kit; N-terminally processed ELISA Kit; NS ELISA Kit; NS3 ELISA Kit; Oncogene KRAS2 ELISA Kit; p21ras ELISA Kit; PR310 c K ras oncogene ELISA Kit; PR310 cK ras oncogene ELISA Kit; RALD ELISA Kit; RASK_HUMAN ELISA Kit; RASK2 ELISA Kit; Transforming protein p21 ELISA Kit; v Ki ras2 Kirsten rat sarcoma 2 viral oncogene homolog ELISA Kit; v Ki ras2 Kirsten rat sarcoma viral oncogene homolog ELISA Kit
Uniprot No.
Homo sapiens (Human)
Sample Types
serum, plasma, tissue homogenates
Detection Range
23.5 pg/mL-1500 pg/mL
5.8 pg/mL
Assay Time
Sample Volume
Detection Wavelength
450 nm
Research Area
Signal Transduction
Assay Principle
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
To assess the linearity of the assay, samples were spiked with high concentrations of human KRAS in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
1:1Average %92
Range %86-102
1:2Average %92
Range %86-108
1:4Average %89
Range %82-98
1:8Average %95
Range %88-100
The recovery of human KRAS spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample TypeAverage % RecoveryRange
Serum (n=5) 9390-97
EDTA plasma (n=4)8883-92
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
15001.756 1.814 1.785 1.631
7501.062 1.123 1.093 0.939
3750.638 0.629 0.634 0.480
187.50.427 0.422 0.425 0.271
940.303 0.317 0.310 0.156
470.254 0.263 0.259 0.105
23.50.196 0.201 0.199 0.045
00.151 0.156 0.154
and FAQs
Store at 2-8°C. Please refer to protocol.
Lead Time
3-5 working days after you place the order, and it takes another 3-5 days for delivery via DHL or FedEx

This Human KRAS ELISA Kit was designed for the quantitative measurement of Human KRAS protein in serum, plasma, tissue homogenates. It is a Sandwich ELISA kit, its detection range is 23.5 pg/mL-1500 pg/mL and the sensitivity is 5.8 pg/mL.

Customer Reviews and Q&A

 Customer Reviews

There are currently no reviews for this product.

Submit a Review here

Target Background

(From Uniprot)
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.
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

Show More

Hide All

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.; [Isoform 2B]: Cell membrane; Lipid-anchor.
Protein Families
Small GTPase superfamily, Ras family
Database Links

HGNC: 6407

OMIM: 190070

KEGG: hsa:3845

STRING: 9606.ENSP00000256078

UniGene: Hs.37003

CUSABIO guaranteed quality
icon of phone
Call us
301-363-4651 (Available 9 a.m. to 5 p.m. CST from Monday to Friday)
icon of address
7505 Fannin St., Ste 610, Room 322 (CUBIO Innovation Center), Houston, TX 77054, USA
icon of social media
Join Us with

Subscribe newsletter

Leave a message

* To protect against spam, please pass the CAPTCHA test below.
CAPTCHA verification
© 2007-2023 CUSABIO TECHNOLOGY LLC All rights reserved. 鄂ICP备15011166号-1