Experts and Doctors on ras proteins in Houston, Texas, United States


Locale: Houston, Texas, United States
Topic: ras proteins

Top Publications

  1. Santarpia L, Lippman S, El Naggar A. Targeting the MAPK-RAS-RAF signaling pathway in cancer therapy. Expert Opin Ther Targets. 2012;16:103-19 pubmed publisher
    ..Further characterization of the RAS-MAPK molecular mechanisms regulation in malignant cells or underlying the acquired resistance to RAF inhibitors will facilitate development of novel combination therapies. ..
  2. Janku F, Lee J, Tsimberidou A, Hong D, Naing A, Falchook G, et al. PIK3CA mutations frequently coexist with RAS and BRAF mutations in patients with advanced cancers. PLoS ONE. 2011;6:e22769 pubmed publisher
    ..001). PIK3CA, RAS (KRAS, NRAS), and BRAF mutations are frequent in diverse tumors. In a wide variety of tumors, PIK3CA mutations coexist with RAS (KRAS, NRAS) and BRAF mutations. ..
  3. Ihle N, Lemos R, Wipf P, Yacoub A, Mitchell C, Siwak D, et al. Mutations in the phosphatidylinositol-3-kinase pathway predict for antitumor activity of the inhibitor PX-866 whereas oncogenic Ras is a dominant predictor for resistance. Cancer Res. 2009;69:143-50 pubmed publisher
  4. Tsao A, Tang X, Sabloff B, Xiao L, Shigematsu H, Roth J, et al. Clinicopathologic characteristics of the EGFR gene mutation in non-small cell lung cancer. J Thorac Oncol. 2006;1:231-9 pubmed
    ..There is a distinct clinical profile for NSCLC patients with the EGFR mutation. However, this mutation does not alter disease-free survival and is likely attributable to an inherited susceptibility instead of an environmental effect. ..
  5. Massarelli E, Varella Garcia M, Tang X, Xavier A, Ozburn N, Liu D, et al. KRAS mutation is an important predictor of resistance to therapy with epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer. Clin Cancer Res. 2007;13:2890-6 pubmed
    ..5% chance of disease progression. KRAS mutation should be included as indicator of resistance in the panel of markers used to predict response to EGFR-TKIs in NSCLC. ..
  6. Riquelme E, Behrens C, Lin H, Simon G, Papadimitrakopoulou V, Izzo J, et al. Modulation of EZH2 Expression by MEK-ERK or PI3K-AKT Signaling in Lung Cancer Is Dictated by Different KRAS Oncogene Mutations. Cancer Res. 2016;76:675-85 pubmed publisher
  7. Wu X, Lippman S. An intermittent approach for cancer chemoprevention. Nat Rev Cancer. 2011;11:879-85 pubmed publisher
    ..This Opinion article provides a detailed discussion of the principle, method and future development of the SITEP approach. ..
  8. McCarthy M, Prakash P, Gorfe A. Computational allosteric ligand binding site identification on Ras proteins. Acta Biochim Biophys Sin (Shanghai). 2016;48:3-10 pubmed publisher
  9. Tan Z, Zhang S. Past, Present, and Future of Targeting Ras for Cancer Therapies. Mini Rev Med Chem. 2016;16:345-57 pubmed
    ..In this article, we will review the progress made in this field and the current state-of-the-art technologies to develop Ras inhibitors. Also we will discuss the future direction of targeting Ras. ..

More Information


  1. Fang B. RAS signaling and anti-RAS therapy: lessons learned from genetically engineered mouse models, human cancer cells, and patient-related studies. Acta Biochim Biophys Sin (Shanghai). 2016;48:27-38 pubmed publisher
    ..Effective subclassifications of RAS mutant cancers may be necessary to improve patients' outcomes through personalized precision medicine. ..
  2. Zhang Y, Du G. Phosphatidic acid signaling regulation of Ras superfamily of small guanosine triphosphatases. Biochim Biophys Acta. 2009;1791:850-5 pubmed publisher
    ..Some future directions and the implication of PA regulation of Ras small GTPases in pathology are also discussed. ..
  3. Janosi L, Gorfe A. Segregation of negatively charged phospholipids by the polycationic and farnesylated membrane anchor of Kras. Biophys J. 2010;99:3666-74 pubmed publisher
  4. Herbst R, Kelly K, Chansky K, Mack P, Franklin W, Hirsch F, et al. Phase II selection design trial of concurrent chemotherapy and cetuximab versus chemotherapy followed by cetuximab in advanced-stage non-small-cell lung cancer: Southwest Oncology Group study S0342. J Clin Oncol. 2010;28:4747-54 pubmed publisher
    ..036). Although both regimens met the efficacy criterion for continued evaluation, the concurrent regimen of paclitaxel/carboplatin plus cetuximab was chosen. ..
  5. Cho K, Park J, Piggott A, Salim A, Gorfe A, Parton R, et al. Staurosporines disrupt phosphatidylserine trafficking and mislocalize Ras proteins. J Biol Chem. 2012;287:43573-84 pubmed publisher
  6. Efuet E, Keyomarsi K. Farnesyl and geranylgeranyl transferase inhibitors induce G1 arrest by targeting the proteasome. Cancer Res. 2006;66:1040-51 pubmed
  7. Prakash P, Zhou Y, Liang H, Hancock J, Gorfe A. Oncogenic K-Ras Binds to an Anionic Membrane in Two Distinct Orientations: A Molecular Dynamics Analysis. Biophys J. 2016;110:1125-38 pubmed publisher
    ..The results suggest that only one of the two major orientation states is capable of effector binding. We propose that the different modes of membrane binding may be exploited in structure-based drug design efforts for cancer therapy. ..
  8. Cho K, Hill M, Chigurupati S, Du G, Parton R, Hancock J. Therapeutic levels of the hydroxmethylglutaryl-coenzyme A reductase inhibitor lovastatin activate ras signaling via phospholipase D2. Mol Cell Biol. 2011;31:1110-20 pubmed publisher
    ..These results suggest that statins modulate key cell signaling pathways as a direct consequence of cholesterol depletion and identify the EGFR-PLD2-Ras-MAPK axis as an important statin target. ..
  9. Donehower L, Creighton C, Schultz N, Shinbrot E, Chang K, Gunaratne P, et al. MLH1-silenced and non-silenced subgroups of hypermutated colorectal carcinomas have distinct mutational landscapes. J Pathol. 2013;229:99-110 pubmed publisher
    ..Examination of MLH1 expression status and frequencies of APC, KRAS, and BRAF mutation in CRC may provide a useful diagnostic tool that could supplement the standard microsatellite instability assays and influence therapeutic decisions. ..
  10. Zhou Y, Cho K, Plowman S, Hancock J. Nonsteroidal anti-inflammatory drugs alter the spatiotemporal organization of Ras proteins on the plasma membrane. J Biol Chem. 2012;287:16586-95 pubmed publisher
    ..This study shows that biological amphiphiles have wide-ranging effects on plasma membrane heterogeneity and protein nanoclustering, revealing a novel mechanism of drug action that has important consequences for cell signaling. ..
  11. Zhou Y, Maxwell K, Sezgin E, Lu M, Liang H, Hancock J, et al. Bile acids modulate signaling by functional perturbation of plasma membrane domains. J Biol Chem. 2013;288:35660-70 pubmed publisher
    ..These observations suggest general, membrane-mediated mechanisms by which biological amphiphiles can produce their cellular effects. ..
  12. Li H, Gorfe A. Aggregation of lipid-anchored full-length H-Ras in lipid bilayers: simulations with the MARTINI force field. PLoS ONE. 2013;8:e71018 pubmed publisher
    ..The simulations also revealed some limitations in the CG force field to study protein assembly in solution, which we discuss in the context of proposed potential avenues of improvement. ..
  13. Iglesias D, Yates M, van der Hoeven D, Rodkey T, Zhang Q, Co N, et al. Another surprise from Metformin: novel mechanism of action via K-Ras influences endometrial cancer response to therapy. Mol Cancer Ther. 2013;12:2847-56 pubmed publisher
    ..These studies provide a rationale for clinical trials using metformin in combination with PI3K-targeted agents for tumors harboring activating K-Ras mutations, and reveal a novel mechanism of action for metformin. ..
  14. Fan H, Richards J. Minireview: physiological and pathological actions of RAS in the ovary. Mol Endocrinol. 2010;24:286-98 pubmed publisher
  15. Ganesan P, Janku F, Naing A, Hong D, Tsimberidou A, Falchook G, et al. Target-based therapeutic matching in early-phase clinical trials in patients with advanced colorectal cancer and PIK3CA mutations. Mol Cancer Ther. 2013;12:2857-63 pubmed publisher
    ..PIK3CA mutations are associated with simultaneous KRAS mutations, possibly accounting for therapeutic resistance. ..
  16. Onken B, Wiener H, Philips M, Chang E. Compartmentalized signaling of Ras in fission yeast. Proc Natl Acad Sci U S A. 2006;103:9045-50 pubmed
    ..These observations provide a striking demonstration of compartment-specific Ras signaling and indicate that spatial specificity in the Ras pathway is evolutionarily conserved. ..
  17. Hennessy B, Gonzalez Angulo A, Stemke Hale K, Gilcrease M, Krishnamurthy S, Lee J, et al. Characterization of a naturally occurring breast cancer subset enriched in epithelial-to-mesenchymal transition and stem cell characteristics. Cancer Res. 2009;69:4116-24 pubmed publisher
    ..PIK3CA mutations, EMT, and stem cell-like characteristics likely contribute to the poor outcomes of MBC and suggest novel therapeutic targets. ..
  18. Zheng Y, Yang W, Xia Y, Hawke D, Liu D, Lu Z. Ras-induced and extracellular signal-regulated kinase 1 and 2 phosphorylation-dependent isomerization of protein tyrosine phosphatase (PTP)-PEST by PIN1 promotes FAK dephosphorylation by PTP-PEST. Mol Cell Biol. 2011;31:4258-69 pubmed publisher
    ..These findings uncover an important mechanism for the regulation of PTP-PEST in activated Ras-induced tumor progression. ..
  19. Wang S, Jabbar K, Lu G, Chen S, Galili N, Vega F, et al. Trisomy 11 in myelodysplastic syndromes defines a unique group of disease with aggressive clinicopathologic features. Leukemia. 2010;24:740-7 pubmed publisher
    ..97). We conclude that trisomy 11 in MDS correlates with clinical aggressiveness, may suggest an early/evolving AML with myelodysplasia-related changes and is best considered a high-risk cytogenetic abnormality in MDS prognostication. ..
  20. Zhao S, Hung F, Colvin J, White A, Dai W, Lovicu F, et al. Patterning the optic neuroepithelium by FGF signaling and Ras activation. Development. 2001;128:5051-60 pubmed
    ..In mouse embryos lacking FGF9, the retinal pigment epithelium extends into the presumptive neural retina, indicating a role of FGF9 in defining the boundary of the neural retina. ..
  21. Tang X, Kadara H, Behrens C, Liu D, Xiao Y, Rice D, et al. Abnormalities of the TITF-1 lineage-specific oncogene in NSCLC: implications in lung cancer pathogenesis and prognosis. Clin Cancer Res. 2011;17:2434-43 pubmed publisher
    ..Our integrative study demonstrates that the protein versus genomic patterns of TITF-1 have opposing roles in lung cancer prognosis and may occur preferentially in different subsets of NSCLC patients with distinct oncogene mutations. ..
  22. Matsuo Y, Campbell P, Brekken R, Sung B, Ouellette M, Fleming J, et al. K-Ras promotes angiogenesis mediated by immortalized human pancreatic epithelial cells through mitogen-activated protein kinase signaling pathways. Mol Cancer Res. 2009;7:799-808 pubmed publisher
  23. Xia C, Ma W, Stafford L, Liu C, Gong L, Martin J, et al. GGAPs, a new family of bifunctional GTP-binding and GTPase-activating proteins. Mol Cell Biol. 2003;23:2476-88 pubmed
    ..Overexpression of GGAPs leads to changes in cell morphology and activation of gene transcription. ..
  24. Maclean J, Rao M, Doyle K, Richards J, Wilkinson M. Regulation of the Rhox5 homeobox gene in primary granulosa cells: preovulatory expression and dependence on SP1/SP3 and GABP. Biol Reprod. 2005;73:1126-34 pubmed
  25. Suehiro Y, Wong C, Chirieac L, Kondo Y, Shen L, Webb C, et al. Epigenetic-genetic interactions in the APC/WNT, RAS/RAF, and P53 pathways in colorectal carcinoma. Clin Cancer Res. 2008;14:2560-9 pubmed publisher
    ..5; P < 0.0002). Our findings suggest that the heterogeneous epigenetic dysregulation of promoter methylation in various genes is interrelated with the occurrence of mutations, as manifested in epigenetic-genetic subgroups of tumors. ..
  26. Shen L, Kondo Y, Rosner G, Xiao L, Hernandez N, Vilaythong J, et al. MGMT promoter methylation and field defect in sporadic colorectal cancer. J Natl Cancer Inst. 2005;97:1330-8 pubmed
    ..13). Some colorectal cancers arise from a field defect defined by epigenetic inactivation of MGMT. Detection of this abnormality may ultimately be useful in risk assessment for colorectal cancer. ..
  27. Henderson Y, Shellenberger T, Williams M, El Naggar A, Fredrick M, Cieply K, et al. High rate of BRAF and RET/PTC dual mutations associated with recurrent papillary thyroid carcinoma. Clin Cancer Res. 2009;15:485-91 pubmed publisher
    ..In addition, the incidence of dual mutations was higher in patients with recurrent PTC than in those primary PTC, as reported by others. ..
  28. Young E, Zheng Z, Wilkins A, Jeong H, Li M, Lichtarge O, et al. Regulation of Ras localization and cell transformation by evolutionarily conserved palmitoyltransferases. Mol Cell Biol. 2014;34:374-85 pubmed publisher
  29. Zuo Z, Chen S, Chandra P, Galbincea J, Soape M, Doan S, et al. Application of COLD-PCR for improved detection of KRAS mutations in clinical samples. Mod Pathol. 2009;22:1023-31 pubmed publisher
    ..In conclusion, we validated the utility and superior sensitivity of COLD-PCR for detecting KRAS mutations in a variety of hematopoietic and solid tumors using either fresh or fixed, paraffin-embedded tissue. ..
  30. Nunez M, Behrens C, Woods D, Lin H, Suraokar M, Kadara H, et al. High expression of folate receptor alpha in lung cancer correlates with adenocarcinoma histology and EGFR [corrected] mutation. J Thorac Oncol. 2012;7:833-40 pubmed publisher
    ..The high levels of FR? in lung adenocarcinomas may be associated to these tumors' better responses to antifolate chemotherapy and represents a potential novel target for this tumor type. ..
  31. Asada S, Choi Y, Yamada M, Wang S, Hung M, Qin J, et al. External control of Her2 expression and cancer cell growth by targeting a Ras-linked coactivator. Proc Natl Acad Sci U S A. 2002;99:12747-52 pubmed
    ..The association of ESX with DRIP130 is mediated by a small hydrophobic face of an 8-aa helix in ESX, suggesting a therapeutic approach to incapacitating the Her2 gene by small organic molecules. ..
  32. Holland E, Celestino J, Dai C, Schaefer L, Sawaya R, Fuller G. Combined activation of Ras and Akt in neural progenitors induces glioblastoma formation in mice. Nat Genet. 2000;25:55-7 pubmed
    ..11), and we show here that Akt activity is increased in most of these tumours, implying that combined activation of these two pathways accurately models the biology of this disease. ..
  33. Park J, Al Ramahi I, Tan Q, Mollema N, Diaz Garcia J, Gallego Flores T, et al. RAS-MAPK-MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1. Nature. 2013;498:325-331 pubmed publisher
    ..Collectively, these data reveal new therapeutic entry points for SCA1 and provide a proof-of-principle for tackling other classes of intractable neurodegenerative diseases. ..
  34. Song S, Ji B, Ramachandran V, Wang H, Hafley M, Logsdon C, et al. Overexpressed galectin-3 in pancreatic cancer induces cell proliferation and invasion by binding Ras and activating Ras signaling. PLoS ONE. 2012;7:e42699 pubmed publisher
    ..These results suggest that Gal-3 contributes to pancreatic cancer progression, in part, by binding Ras and activating Ras signaling. Gal-3 may therefore be a potential novel target for this deadly disease. ..
  35. Janku F, Wheler J, Naing A, Stepanek V, Falchook G, Fu S, et al. PIK3CA mutations in advanced cancers: characteristics and outcomes. Oncotarget. 2012;3:1566-75 pubmed
    ..PIK3CA mutations, especially, H1047R, were associated with attaining a PR/CR to PI3K/AKT/mTOR pathway inhibitors. ..
  36. Prokopenko S, Saint R, Bellen H. Untying the Gordian knot of cytokinesis. Role of small G proteins and their regulators. J Cell Biol. 2000;148:843-8 pubmed
  37. Yom S, Rashid A, Rosenthal D, Elliott D, Hanna E, Weber R, et al. Genetic analysis of sinonasal adenocarcinoma phenotypes: distinct alterations of histogenetic significance. Mod Pathol. 2005;18:315-9 pubmed
  38. Yen H, Gordon C, Chang E. Schizosaccharomyces pombe Int6 and Ras homologs regulate cell division and mitotic fidelity via the proteasome. Cell. 2003;112:207-17 pubmed
    ..We propose that human Int6, either alone or cooperatively with Ras, influences proteasome activities via Rpn5. Inactivating Int6 can lead to accumulation of mitotic regulators affecting cell division and mitotic fidelity. ..
  39. Wong K. Recent developments in anti-cancer agents targeting the Ras/Raf/ MEK/ERK pathway. Recent Pat Anticancer Drug Discov. 2009;4:28-35 pubmed
    ..In this review, we will discuss new patents or patent applications related to inhibitors of the Ras/Raf/MEK/ERK pathway. ..
  40. Lacaria M, Gu W, Lupski J. Circadian abnormalities in mouse models of Smith-Magenis syndrome: evidence for involvement of RAI1. Am J Med Genet A. 2013;161A:1561-8 pubmed publisher
    ..This study also confirms a previous report of abnormal circadian function in Dexras1(-/-) mice. ..
  41. Seguin L, Kato S, Franovic A, Camargo M, Lesperance J, Elliott K, et al. An integrin β₃-KRAS-RalB complex drives tumour stemness and resistance to EGFR inhibition. Nat Cell Biol. 2014;16:457-68 pubmed publisher
    ..These findings not only identify α(v)β₃ as a marker/driver of carcinoma stemness but also reveal a therapeutic strategy to sensitize such tumours to RTK inhibition. ..
  42. Valentin Vega Y, Okano H, Lozano G. The intestinal epithelium compensates for p53-mediated cell death and guarantees organismal survival. Cell Death Differ. 2008;15:1772-81 pubmed publisher
    ..While Mdm2 is a critical inhibitor of p53 in the intestinal epithelium, the tissue employs a series of processes that compensate for cell death. ..
  43. Fan H, Liu Z, Mullany L, Richards J. Consequences of RAS and MAPK activation in the ovary: the good, the bad and the ugly. Mol Cell Endocrinol. 2012;356:74-9 pubmed publisher
    ..These diverse effects of RAS highlight how critical its activation is linked to cell- and stage-specific events in the ovary that control normal processes and that can also lead to altered granulosa cell and OSE cell fates. ..
  44. Cheung L, Hennessy B, Li J, Yu S, Myers A, Djordjevic B, et al. High frequency of PIK3R1 and PIK3R2 mutations in endometrial cancer elucidates a novel mechanism for regulation of PTEN protein stability. Cancer Discov. 2011;1:170-85 pubmed publisher
    ..Taken together, the PI3K pathway represents a critical driver of endometrial cancer pathogenesis and a novel therapeutic target. ..
  45. van der Hoeven D, Cho K, Ma X, Chigurupati S, Parton R, Hancock J. Fendiline inhibits K-Ras plasma membrane localization and blocks K-Ras signal transmission. Mol Cell Biol. 2013;33:237-51 pubmed publisher
    ..Taken together, these results suggest that inhibitors of K-Ras plasma membrane localization may have utility as novel K-Ras-specific anticancer therapeutics...
  46. Agarwal R, Jurisica I, Mills G, Cheng K. The emerging role of the RAB25 small GTPase in cancer. Traffic. 2009;10:1561-8 pubmed publisher
    ..Here, we review the link between RAB25 and tumor development and current knowledge regarding its possible roles in cancer. ..
  47. Lin S, Elledge S. Multiple tumor suppressor pathways negatively regulate telomerase. Cell. 2003;113:881-9 pubmed
    ..These studies suggest that multiple tumor suppressor/oncogene pathways coordinately repress hTERT expression and imply that telomerase is reactivated in human tumors through oncogenic mutations. ..
  48. Woodfield S, Zhang L, Scorsone K, Liu Y, Zage P. Binimetinib inhibits MEK and is effective against neuroblastoma tumor cells with low NF1 expression. BMC Cancer. 2016;16:172 pubmed publisher
    ..MEK inhibition therefore represents a potential new therapeutic strategy for neuroblastoma. ..
  49. Feng W, Brown R, Trung C, Li W, Wang L, Khoury T, et al. Morphoproteomic profile of mTOR, Ras/Raf kinase/ERK, and NF-kappaB pathways in human gastric adenocarcinoma. Ann Clin Lab Sci. 2008;38:195-209 pubmed
  50. Douillard J, Shepherd F, Hirsh V, Mok T, Socinski M, Gervais R, et al. Molecular predictors of outcome with gefitinib and docetaxel in previously treated non-small-cell lung cancer: data from the randomized phase III INTEREST trial. J Clin Oncol. 2010;28:744-52 pubmed publisher
  51. Deqin M, Chen Z, Nero C, Patel K, Daoud E, Cheng H, et al. Somatic deletions of the polyA tract in the 3' untranslated region of epidermal growth factor receptor are common in microsatellite instability-high endometrial and colorectal carcinomas. Arch Pathol Lab Med. 2012;136:510-6 pubmed publisher
    ..Deletions of EGFR 3' UTR polyA are frequent in endometrial and colorectal carcinomas, are confined almost exclusively to MSI-H tumors, and do not affect KRAS and BRAF mutations. ..
  52. Atreya C, Corcoran R, Kopetz S. Expanded RAS: refining the patient population. J Clin Oncol. 2015;33:682-5 pubmed publisher
  53. Lee S, Kunz J, Lin S, Yu Lee L. 16-kDa prolactin inhibits endothelial cell migration by down-regulating the Ras-Tiam1-Rac1-Pak1 signaling pathway. Cancer Res. 2007;67:11045-53 pubmed
    ..Thus, 16k PRL inhibits cell migration by blocking the Ras-Tiam1-Rac1-Pak1 signaling pathway in endothelial cells. ..
  54. Yang G, Rosen D, Zhang Z, Bast R, Mills G, Colacino J, et al. The chemokine growth-regulated oncogene 1 (Gro-1) links RAS signaling to the senescence of stromal fibroblasts and ovarian tumorigenesis. Proc Natl Acad Sci U S A. 2006;103:16472-7 pubmed
    ..Therefore, Gro-1 may be a therapeutic target as well as a diagnostic marker in ovarian cancer. ..
  55. Vauthey J, Zimmitti G, Kopetz S, Shindoh J, Chen S, Andreou A, et al. RAS mutation status predicts survival and patterns of recurrence in patients undergoing hepatectomy for colorectal liver metastases. Ann Surg. 2013;258:619-26; discussion 626-7 pubmed publisher
    ..181). RAS mutation predicts early lung recurrence and worse survival after curative resection of CLM. This information may be used to individualize systemic and local tumor-directed therapies and follow-up strategies. ..
  56. Chandra P, Luthra R, Zuo Z, Yao H, Ravandi F, Reddy N, et al. Acute myeloid leukemia with t(9;11)(p21-22;q23): common properties of dysregulated ras pathway signaling and genomic progression characterize de novo and therapy-related cases. Am J Clin Pathol. 2010;133:686-93 pubmed publisher
    ..Ras activation seems to complement the MLLT3-MLL oncogene in transformation with features of de novo and t-AML with MLLT3-MLL being similar. ..
  57. Kahlert C, Melo S, Protopopov A, Tang J, Seth S, Koch M, et al. Identification of double-stranded genomic DNA spanning all chromosomes with mutated KRAS and p53 DNA in the serum exosomes of patients with pancreatic cancer. J Biol Chem. 2014;289:3869-75 pubmed publisher
    ..These results indicate that serum-derived exosomes can be used to determine genomic DNA mutations for cancer prediction, treatment, and therapy resistance. ..
  58. Tong C, Ohyama T, Tien A, Rajan A, Haueter C, Bellen H. Rich regulates target specificity of photoreceptor cells and N-cadherin trafficking in the Drosophila visual system via Rab6. Neuron. 2011;71:447-59 pubmed publisher
    ..The active form of Rab6 strongly suppresses the rich synaptic specificity defect, indicating that Rab6 is regulated by Rich. We propose that Rich activates Rab6 to regulate N-Cadherin trafficking and affects synaptic specificity. ..
  59. Wilson Rawls J, Liu J, Laneuville P, Arlinghaus R. P210 Bcr-Abl interacts with the interleukin-3 beta c subunit and constitutively activates Jak2. Leukemia. 1997;11 Suppl 3:428-31 pubmed
    ..Previously, it has been demonstrated that Bcr-Abl interacts with Grb2 and Shc, which in turn activates the Ras pathway. Thus, Bcr-Abl can activate signalling through both pathways in a factor-independent fashion. ..
  60. Takada Y, Khuri F, Aggarwal B. Protein farnesyltransferase inhibitor (SCH 66336) abolishes NF-kappaB activation induced by various carcinogens and inflammatory stimuli leading to suppression of NF-kappaB-regulated gene expression and up-regulation of apoptosis. J Biol Chem. 2004;279:26287-99 pubmed
  61. Li Y, Chang E. Schizosaccharomyces pombe Ras1 effector, Scd1, interacts with Klp5 and Klp6 kinesins to mediate cytokinesis. Genetics. 2003;165:477-88 pubmed
    ..These data suggest that Klp5/6 cooperate with the Ras1-Scd1 pathway to influence proper formation of the contractile ring for cytokinesis. ..
  62. Dunlap S, Celestino J, Wang H, Jiang R, Holland E, Fuller G, et al. Insulin-like growth factor binding protein 2 promotes glioma development and progression. Proc Natl Acad Sci U S A. 2007;104:11736-41 pubmed
    ..Thus, this study provides definitive evidence that IGFBP2 plays a key role in activation of the Akt pathway and collaborates with K-Ras or PDGFB in the development and progression of two major types of glioma. ..
  63. Lindsey J. Dexamethasone-induced Ras-related protein 1 is a potential regulatory protein in B lymphocytes. Int Immunol. 2007;19:583-90 pubmed
    ..We conclude that Rasd1 mRNA is expressed by B lymphocytes derived from lymph node cells in response to inactivating or inhibitory stimuli. It may play a role in regulating B lymphocyte activity and proliferation. ..
  64. Liou J, Matijevic Aleksic N, Lee S, Wu K. Prostacyclin inhibits endothelial cell XIAP ubiquitination and degradation. J Cell Physiol. 2007;212:840-8 pubmed
    ..Preservation of XIAP proteins represents a key mechanism by which PGI(2) protects endothelial cells from oxidant-induced apoptosis. ..
  65. Johnson C, Chun Jen Lin C, Stern M. Ras-dependent and Ras-independent effects of PI3K in Drosophila motor neurons. Genes Brain Behav. 2012;11:848-58 pubmed publisher
    ..In contrast, the ability of PI3K to increase nerve terminal growth is Ras-independent. These results suggest that distinct regulatory mechanisms underlie the effects of PI3K on distinct phenotypic outputs. ..
  66. Fan H, Shimada M, Liu Z, Cahill N, Noma N, Wu Y, et al. Selective expression of KrasG12D in granulosa cells of the mouse ovary causes defects in follicle development and ovulation. Development. 2008;135:2127-37 pubmed publisher
    ..Transient but not sustained activation of RAS in granulosa cells is therefore crucial for directing normal follicle development and initiating the ovulation process. ..
  67. Solis L, Raso M, Kalhor N, Behrens C, Wistuba I, Moran C. Primary oncocytic adenocarcinomas of the lung: a clinicopathologic, immunohistochemical, and molecular biologic analysis of 16 cases. Am J Clin Pathol. 2010;133:133-40 pubmed publisher
    ..These cases represent an unusual variant of pulmonary adenocarcinoma. ..
  68. Johnson F, Bekele B, Feng L, Wistuba I, Tang X, Tran H, et al. Phase II study of dasatinib in patients with advanced non-small-cell lung cancer. J Clin Oncol. 2010;28:4609-15 pubmed publisher
    ..Marked activity in one patient and prolonged stable disease in four others suggested a potential subpopulation of patients with dasatinib-sensitive NSCLC. ..
  69. Barboza J, Liu G, Ju Z, El Naggar A, Lozano G. p21 delays tumor onset by preservation of chromosomal stability. Proc Natl Acad Sci U S A. 2006;103:19842-7 pubmed
    ..Thus, p21 coupled p53-dependent checkpoint control and preservation of chromosomal stability, and cooperated with apoptosis in suppressing tumor onset in mice. ..
  70. Sarkar P, Hayes B. Induction of COX-2 by acrolein in rat lung epithelial cells. Mol Cell Biochem. 2007;301:191-9 pubmed
    ..The results of these studies offer an explanation for the mechanism of COX-2 induction by acrolein in rat lung epithelial cells. ..
  71. Yang Z, Barnes C, Kumar R. Human epidermal growth factor receptor 2 status modulates subcellular localization of and interaction with estrogen receptor alpha in breast cancer cells. Clin Cancer Res. 2004;10:3621-8 pubmed
  72. Garrido Laguna I, Hong D, Janku F, Nguyen L, Falchook G, Fu S, et al. KRASness and PIK3CAness in patients with advanced colorectal cancer: outcome after treatment with early-phase trials with targeted pathway inhibitors. PLoS ONE. 2012;7:e38033 pubmed publisher
    ..KRAS and PIK3CA mutations frequently coexist in patients with colorectal cancer, and are associated with clinical characteristics and outcome. Overcoming resistance may require targeting both pathways. ..
  73. Richards J, Fan H, Liu Z, Tsoi M, Laguë M, Boyer A, et al. Either Kras activation or Pten loss similarly enhance the dominant-stable CTNNB1-induced genetic program to promote granulosa cell tumor development in the ovary and testis. Oncogene. 2012;31:1504-20 pubmed publisher
    ..Importantly, the results provide strong evidence that CTNNB1 is the driver in these contexts and that KRAS(G12D) and Pten loss promote the program set in motion by the CTNNB1. ..
  74. Chang B, Liu G, Yang G, Mercado Uribe I, Huang M, Liu J. REDD1 is required for RAS-mediated transformation of human ovarian epithelial cells. Cell Cycle. 2009;8:780-6 pubmed
    ..Our data demonstrated that REDD1 is a key mediator in RAS-mediated transformation through an effect on anti-apoptosis. ..
  75. Zheng Y, Xia Y, Hawke D, Halle M, Tremblay M, Gao X, et al. FAK phosphorylation by ERK primes ras-induced tyrosine dephosphorylation of FAK mediated by PIN1 and PTP-PEST. Mol Cell. 2009;35:11-25 pubmed publisher
    ..These findings uncover the importance of sequential modification of FAK-by serine phosphorylation, isomerization, and tyrosine dephosphorylation--in the regulation of FAK activity and, thereby, in Ras-related tumor metastasis. ..
  76. Caldwell P, Walkiewicz M, Stern M. Ras activity in the Drosophila prothoracic gland regulates body size and developmental rate via ecdysone release. Curr Biol. 2005;15:1785-95 pubmed
    ..We also suggest that ecdysone release is regulated in two ways: a PI3K-dependent growth-promoting effect on PG cells, and a Raf-dependent step that may involve the transcriptional regulation of ecdysone biosynthetic genes. ..
  77. Greene V, Johnson M, Grimm E, Ellerhorst J. Frequencies of NRAS and BRAF mutations increase from the radial to the vertical growth phase in cutaneous melanoma. J Invest Dermatol. 2009;129:1483-8 pubmed publisher
    ..JID JOURNAL CLUB ARTICLE: For questions, answers, and open discussion about this article, please go to ..