The role of p19 and p21 H-Ras proteins and mutants in miRNA expression in cancer and a Costello syndrome cell model
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C. Croce | Chang-gong Liu | S. Volinia | G. Calin | C. Taccioli | M. Bach-Elias | Maria Camats | Roseli García-Cruz
[1] You Li,et al. MiR-206, a Key Modulator of Skeletal Muscle Development and Disease , 2015, International journal of biological sciences.
[2] C. Niemeyer. RAS diseases in children , 2014, Haematologica.
[3] G. Schratt,et al. MicroRNA-132, -134, and -138: a microRNA troika rules in neuronal dendrites , 2014, Cellular and Molecular Life Sciences.
[4] H. Harn,et al. Therapeutic Potential of MicroRNA Let-7: Tumor Suppression or Impeding Normal Stemness , 2014, Cell transplantation.
[5] P. Fergelot,et al. Cutaneous Manifestations in Costello and Cardiofaciocutaneous Syndrome: Report of 18 Cases and Literature Review , 2013, Pediatric dermatology.
[6] N. Selvamurugan,et al. Regulation of Breast Cancer and Bone Metastasis by MicroRNAs , 2013, Disease markers.
[7] S. Knuutila,et al. MicroRNA Profiling in Chemoresistant and Chemosensitive Acute Myeloid Leukemia , 2013, Cytogenetic and Genome Research.
[8] D. Faller,et al. Targeting the RAS oncogene , 2013, Expert opinion on therapeutic targets.
[9] A. Tamura,et al. Crystal structures of the state 1 conformations of the GTP‐bound H‐Ras protein and its oncogenic G12V and Q61L mutants , 2012, FEBS letters.
[10] C. Deltas,et al. microRNAs: a newly described class of encoded molecules that play a role in health and disease. , 2010, Hippokratia.
[11] C. Angelini,et al. Overexpression of microRNA-206 in the skeletal muscle from myotonic dystrophy type 1 patients , 2010, Journal of Translational Medicine.
[12] Chul-Hong Kim,et al. p19(ras) Represses proliferation of non-small cell lung cancer possibly through interaction with Neuron-Specific Enolase (NSE). , 2010, Cancer letters.
[13] G. Brewer,et al. Impairment of mitochondrial respiration in mouse fibroblasts byoncogenic H-RASQ61L , 2010, Cancer biology & therapy.
[14] K. Heesom,et al. P19 H-Ras Induces G1/S Phase Delay Maintaining Cells in a Reversible Quiescence State , 2009, PloS one.
[15] Zsolt Czimmerer,et al. DIFFERENTIALLY EXPRESSED MicroRNAs IN SMALL CELL LUNG CANCER , 2009, Experimental lung research.
[16] D. Kaplan,et al. Costello syndrome H-Ras alleles regulate cortical development. , 2009, Developmental biology.
[17] F. Slack,et al. let-7 microRNAs in development, stem cells and cancer. , 2008, Trends in molecular medicine.
[18] Jung-Woong Kim,et al. p19(ras) amplifies p73beta-induced apoptosis through mitochondrial pathway. , 2008, Biochemical and biophysical research communications.
[19] K. Gripp,et al. Clarification of previously reported Costello syndrome patients , 2008, American journal of medical genetics. Part A.
[20] W. Gerald,et al. Endogenous human microRNAs that suppress breast cancer metastasis , 2008, Nature.
[21] C. Croce,et al. MicroRNA gene expression during retinoic acid-induced differentiation of human acute promyelocytic leukemia , 2007, Oncogene.
[22] B. White,et al. The Micro-Ribonucleic Acid (miRNA) miR-206 Targets the Human Estrogen Receptor-α (ERα) and Represses ERα Messenger RNA and Protein Expression in Breast Cancer Cell Lines , 2007 .
[23] J. Rivas,et al. Transcriptional networks of knockout cell lines identify functional specificities of H-Ras and N-Ras: significant involvement of N-Ras in biotic and defense responses , 2007, Oncogene.
[24] J. Hoffman,et al. Somatic mosaicism for an HRAS mutation causes Costello syndrome , 2006, American journal of medical genetics. Part A.
[25] K. Gripp,et al. Paternal bias in parental origin of HRAS mutations in Costello syndrome , 2006, Human mutation.
[26] O. Dereure. Mutations du proto-oncogène H-Ras dans le syndrome de Costello , 2006 .
[27] Yukichi Tanaka,et al. Germline mutations in HRAS proto-oncogene cause Costello syndrome , 2005, Nature Genetics.
[28] Krister Wennerberg,et al. The Ras superfamily at a glance , 2005, Journal of Cell Science.
[29] C. Croce,et al. An oligonucleotide microchip for genome-wide microRNA profiling in human and mouse tissues. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[30] S. Guil,et al. Roles of hnRNP A1, SR Proteins, and p68 Helicase in c-H-ras Alternative Splicing Regulation , 2003, Molecular and Cellular Biology.
[31] Thomas D. Schmittgen,et al. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. , 2001, Methods.
[32] M. Malumbres,et al. Targeted Genomic Disruption of H-ras and N-ras, Individually or in Combination, Reveals the Dispensability of Both Loci for Mouse Growth and Development , 2001, Molecular and Cellular Biology.
[33] L. Peso,et al. The Ras family of GTPases in cancer cell invasion , 2000, Cellular and Molecular Life Sciences CMLS.
[34] A. Levinson,et al. Expression of the H-ras proto-oncogene is controlled by alternative splicing , 1989, Cell.
[35] A. Levinson,et al. A point mutation in the last intron responsible for increased expression and transforming activity of the c-Ha-ras oncogene , 1988, Nature.
[36] X. Wan,et al. Expression of the tumor suppressor miR-206 is associated with cellular proliferative inhibition and impairs invasion in ERα-positive endometrioid adenocarcinoma. , 2012, Cancer letters.
[37] B. White,et al. The micro-ribonucleic acid (miRNA) miR-206 targets the human estrogen receptor-alpha (ERalpha) and represses ERalpha messenger RNA and protein expression in breast cancer cell lines. , 2007, Molecular endocrinology.
[38] O. Dereure. [Mutations in H-Ras proto-oncogen in Costello syndrome]. , 2006, Annales de dermatologie et de venereologie.
[39] E. Zackai,et al. HRAS mutation analysis in Costello syndrome: Genotype and phenotype correlation , 2006, American journal of medical genetics. Part A.
[40] J. Ferrer,et al. Alternative splicing of the human proto-oncogene c-H-ras renders a new Ras family protein that trafficks to cytoplasm and nucleus. , 2003, Cancer research.
[41] D. Lowy,et al. Function and regulation of ras. , 1993, Annual review of biochemistry.