Recombinant Mouse GTPase KRas (Kras)

1. GATAD2B interacts with C-MYC to enhance KRAS driven tumor growth. PMID: 30013058
2. In mice that express activated KRAS in the pancreas, we found expression of GNAS(R201C) to cause development of more differentiated tumors, with gene expression pattern associated with the ductal phenotype. PMID: 30142336
3. 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
4. gene expression profiles of each of the Ras isoforms in a panel of mouse tissues derived from a full developmental time course, are reported. PMID: 28117393
5. The results show that genetic abrogation of Nrf2 impairs the malignant phenotype of K-Ras-transformed cells in vitro and in vivo, and demonstrates the critical role of Nrf2 in promoting cell survival and drug resistance in cells harboring oncogenic K-ras. PMID: 29621903
6. 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
7. 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
8. transgenic mice expressing Slug and Kras in acinar cells were generated. Surprisingly, Slug attenuated Kras-induced acinar-ductal metaplasia (ADM)development, ERK1/2 phosphorylation and proliferation. Co-expression of Slug with Kras also attenuated chronic pancreatitis-induced changes in ADM development and fibrosis PMID: 27364947
9. PTEN loss and activated Kras have synergistic effects in promoting development of intraductal papillary mucinous neoplasms and progression to pancreatic ductal adenocarcinoma. PMID: 29273451
10. Given the significance of KRAS activity as a driver in tumorigenesis, identification of K147 acetylation as a novel post-translational modification directed by SIRT2 in vivo may provide a better understanding of the mechanistic link regarding the crosstalk between non-genetic and genetic factors in KRAS driven tumors. PMID: 27637077
11. KY1022, a small molecule that destabilizes both beta-catenin and Ras by targeting the Wnt/beta-catenin pathway, inhibitits cellular events, including epithelial mesenchymal transformation, an initial process of metastasis, and apoptosis in colorectal cancer cells. PMID: 27835580
12. ACSL3 is essential for mutant KRAS lung cancer tumorigenesis in vivo and is highly expressed in human lung cancer PMID: 27477280
13. Neurofibromin regulates macrophage superoxide production via p21Ras.Neurofibromin-deficient smooth muscle cells are sensitive to oxidative stress.NADPH oxidase 2 is required for NF1 arterial stenosis.Neurofibromatosis type 1 patients have evidence of chronic oxidative stress. PMID: 27266634
14. RAS signaling can upregulate tumor cell PD-L1 expression through a mechanism involving increases in PD-L1 mRNA stability via modulation of the AU-rich element-binding protein tristetraprolin. PMID: 29246442
15. In a mouse lung model of KRas(G12D)-driven adenomas, co-activation of Myc drives the immediate transition to highly proliferative and invasive adenocarcinomas marked by highly inflammatory, angiogenic, and immune-suppressed stroma. PMID: 29195074
16. Interactions between the Wnt/beta-catenin and the Kras/ERK/Foxm1 pathways are essential to restrict SOX9 expression in basal cells during pulmonary branching morphogenesis PMID: 26869074
17. Data show that the induction of BIM in the MYC- and RAS-driven leukemia is mediated by the downregulation of miR-17-92, and suggest that induction of BIM-mediated apoptosis may be a therapeutic approach for acute lymphoblastic leukemia (ALL). PMID: 27095570
18. Data show that cisplatin response was enhanced in human lung cancer cells when Nit1 was knocked down and mice Nit1-/-:KrasG12D/+ tumors showed increased sensitivity to cisplatin in vivo. PMID: 26967383
19. that Kras is a major regulator of TPO and GM-CSF signaling in specific populations of hematopoietic cells. PMID: 26972179
20. We crossed Ptf1a(Cre/+) ;Kras(G12D/+) mice with JNK1(-/-) mice to generate Ptf1a(Cre/+) ;Kras(G12D/+) ;JNK1(-/-) (Kras;JNK1(-/-) ) mice. Tumor weight was significantly lower in Kras;JNK1(-/-) mice than in Kras;JNK1(+/-) mice, whereas histopathological features were similar.we concluded that inhibition of activated JNK in pancreatic tumor stroma could be a potential therapeutic target to increase Ccl20 secretion PMID: 28837246
21. Transgenic mouse line expressing the human Ki-Ras bearing an activating mutation (Ki-Ras((G12V))) selectively in the mammary epithelium develop estrogen receptor alpha (ERalpha)-positive ductal adenocarcinomas with 100% incidence within 3-9 months after Ki-Ras((G12V)) induction. PMID: 28745321
22. It has been concluded that VMP1-mediated autophagy cooperated with Kras to promote pancreatic ductal adenocarcinoma initiation. PMID: 27415425
23. High KRAS expression is associated with Gastric Tumorigenesis. PMID: 28760854
24. Study underscores genomic alterations that represent early events in the development of Kras mutant LUAD following Gprc5a loss and tobacco carcinogen exposure. PMID: 28653505
25. a KrasG12D mouse model that reproducibly develops JMML-like disease. This model will prove useful for preclinical drug studies and for elucidating the developmental origins of pediatric neoplasms. PMID: 28846072
26. In the absence of TP53, chronic imflammaiton leads to the development of several rare K-ras-independent forms of PC, with infrequent PDAC. PMID: 27991926
27. KrasG12D-driven proliferation of pancreatic ductal epithelial cells (PDECs) depends on an EGFR signaling loop engaging the oncogenic transcription factor c-MYC. PMID: 26592448
28. median survival of KPIC mice was longer than that of LSL-KrasG12D; Ink4flox/flox; Ptf1/p48-Cre mice (KIC) (89 vs 62 days) and shorter than that of KRAS (KrasG12D), TP53 (Trp53R172H/+) and Ptf1/p48-Cre (KPC) mice PMID: 28475592
29. Loss of N-cadherin in the context of oncogenic K-ras leads to increased pancreatic intraepithelial neoplasia (PanIN) incidence and progression. PMID: 26477318
30. activating mutations in GNAS and Kras cooperatively promote murine pancreatic tumorigenesis PMID: 26257060
31. the Kras(mut) allele was heterogenous in primary tumors yet homogenous in metastases, a pattern consistent with activated Kras(mut) signaling being a driver of progression to metastasis. PMID: 28289141
32. Using an extensive collection of novel murine cell lines we have identified distinct roles for Kras and Pten on MUC1 and EMT in vivo and in vitro. The data has implications for future design of combination therapies targeting Kras mutations, Pten deletions and MUC1 vaccines. PMID: 26973247
33. a potent tumor-suppressive function for Lfng PMID: 26279302
34. pancreatic ductal cells, whereas exhibiting relative resistance to oncogenic Kras alone, can serve as an effective cell of origin for pancreatic ductal adenocarcinoma in the setting of gain-of-function mutations in p53 PMID: 26592447
35. In vivo treatment of the KRAS(G12D)-induced Langerhans cell histiocytosis -like mouse with the cholesterol-lowering drug atorvastatin ameliorated the pathology, implicating statins as potential therapeutics against a subset of pulmonary Langerhans cell histiocytosis. PMID: 28550040
36. overactivation of Kras signaling in type II collagen-positive, immature osteoprogenitor cells, but not in mature osteoblasts, substantially increases the number of their descendant stromal cells and mature osteoblasts, and subsequently increases bone mass. PMID: 27735946
37. demonstrate the tumor suppressor function of WT Kras in oncogenic Kras-induced leukemogenesis and elucidate its underlying cellular and signaling mechanisms. PMID: 27055865
38. Modification of the tumor microenvironment in KRAS or c-MYC-induced ovarian cancer-associated peritonitis has been described. PMID: 27483433
39. we provide genetic evidence that the wild-type H-Ras and K-Ras proteins are bioequivalent in spite of their different structural and biological properties PMID: 27872088
40. KRAS K104Q mutant exhibited defects in both guanine nucleotide exchange factors -mediated exchange and GTPase-activating proteins -mediated GTP hydrolysis, consistent with NMR-detected structural perturbations in localized regions of KRAS important for recognition of these regulatory proteins. PMID: 28154176
41. farnesylation of K-Ras was required for its packaging within extracellular nanovesicles, yet expressing a K-Ras farnesylation mutant did not decrease the number of nanovesicles or the amount of Alix protein released per cell. PMID: 27909058
42. The K-Ras(V14I) activating protein is able to induce cancer, although at a much lower level than the classical K-Ras(G12V) oncogene, and that it can be significantly modulated by both genetic and non-genetic events. PMID: 27174785
43. Gli1 and Gli2 exhibited different functions in the regulation of p63 expression or proliferation of p63(+) cells in Kras-AR driven tumors. PMID: 27760825
44. our data suggest that GGPPS is essential for maintaining fetal lung branching morphogenesis, which is possibly through regulating K-Ras prenylation. PMID: 27106761
45. We establishment the transgenic mouse model of K-ras(G12D) p53(loxP/loxP) and found that K-ras mutation and p53 deletion within the ovarian surface epithelium gave rise to ovarian lesions with a hyperproliferation and endometrioid glandular morphology PMID: 28032649
46. the expression of EGFRL858R in KrasG12V-driven lung adenocarcinoma limits tumor progression due to the induction of a transient oncogenic conflict PMID: 27775074
47. K-Ras knockout (KO) mouse embryonic fibroblasts (K-ras(-/-) ) stimulated with transforming growth factor-beta1 (TGF-beta1) exhibited reduced proliferation and impaired mobility than wild-type fibroblasts PMID: 26873620
48. findings demonstrate that advanced gastric tumorigenesis requires oncogenic KRAS or BRAF in concert with aberrant STAT3 activation in epithelial precursor cells of the glandular stomach PMID: 26837764
49. oncogenic KRas-induced increase in fluid-phase endocytosis has a key role during cellular transdifferentiation in pancreatic acinar cells. This result supports emerging evidence for endocytosis playing a crucial role in regulating the signaling output of the cells PMID: 28057438
50. This study reveals KRAS(G12D) uniquely regulates tumor cells via heterotypic stromal cells. By exploiting heterocellularity, reciprocal signaling enables KRAS(G12D) to engage oncogenic signaling pathways beyond those regulated in a cell-autonomous manner. PMID: 27087446

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KEGG: mmu:16653

STRING: 10090.ENSMUSP00000032399

UniGene: Mm.383182