نتایج جستجو برای: مسیر ras

تعداد نتایج: 54191  

Journal: :Blood 2009
Jeffrey W Tyner Heidi Erickson Michael W N Deininger Stephanie G Willis Christopher A Eide Ross L Levine Michael C Heinrich Norbert Gattermann D Gary Gilliland Brian J Druker Marc M Loriaux

Transforming mutations in NRAS and KRAS are thought to play a causative role in the development of numerous cancers, including myeloid malignancies. Although mutations at amino acids 12, 13, or 61 account for the majority of oncogenic Ras variants, we hypothesized that less frequent mutations at alternate residues may account for disease in some patients with cancer of unexplained genetic etiol...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2012
Yihua Wang Xiao Dan Wang Eleonora Lapi Alexandra Sullivan Wei Jia You-Wen He Indrika Ratnayaka Shan Zhong Robert D Goldin Christoph G Goemans Aviva M Tolkovsky Xin Lu

RAS is frequently mutated in human cancers and has opposing effects on autophagy and tumorigenesis. Identifying determinants of the cellular responses to RAS is therefore vital in cancer research. Here, we show that autophagic activity dictates the cellular response to oncogenic RAS. N-terminal Apoptosis-stimulating of p53 protein 2 (ASPP2) mediates RAS-induced senescence and inhibits autophagy...

2016
Haibo Zhang Ji Luo

This review discusses our current understanding of the small ubiquitin-like modifier (SUMO) pathway and how it functionally intersects with Ras signaling in cancer. The Ras family of small GTPases are frequently mutated in cancer. The role of the SUMO pathway in cancer and in Ras signaling is currently not well understood. Recent studies have shown that the SUMO pathway can both regulate Ras/MA...

2002
Giovanni Cuda Roberto Ceravolo Francesco Perticone Maria Concetta Faniello Antonio Ruocco Enrico V. Avvedimento

Background—Reactive oxygen species play a critical role in inducing apoptosis. The small GTPase p21 Ras and the ERK1/2 MAPK have been proposed as key regulators of the signaling cascade triggered by oxidative stress (H2O2). Harvey-Ras (Ha-Ras) and Kirsten-Ras (Ki-Ras) isoforms are so far functionally indistinguishable, because they activate the same downstream effectors, including ERK1/2. Moreo...

Journal: :Circulation 2002
Giovanni Cuda Roberto Paternò Roberto Ceravolo Mafalda Candigliota Nicola Perrotti Francesco Perticone Maria Concetta Faniello Filippo Schepis Antonio Ruocco Evelina Mele S Cassano Maurizio Bifulco Mariarosaria Santillo Enrico V Avvedimento

BACKGROUND Reactive oxygen species play a critical role in inducing apoptosis. The small GTPase p21 Ras and the ERK1/2 MAPK have been proposed as key regulators of the signaling cascade triggered by oxidative stress (H2O2). Harvey-Ras (Ha-Ras) and Kirsten-Ras (Ki-Ras) isoforms are so far functionally indistinguishable, because they activate the same downstream effectors, including ERK1/2. Moreo...

2011
Clara L. Oeste Beatriz Díez-Dacal Francesca Bray Mario García de Lacoba Beatriz G. de la Torre David Andreu Antonio J. Ruiz-Sánchez Ezequiel Pérez-Inestrosa Carlota A. García-Domínguez José M. Rojas Dolores Pérez-Sala

Ras proteins are crucial players in differentiation and oncogenesis and constitute important drug targets. The localization and activity of Ras proteins are highly dependent on posttranslational modifications at their C-termini. In addition to an isoprenylated cysteine, H-Ras, but not other Ras proteins, possesses two cysteine residues (C181 and C184) in the C-terminal hypervariable domain that...

Journal: :BMC Gastroenterology 2008
Charles E Patek Mark J Arends Lorraine Rose Feijun Luo Marion Walker Paul S Devenney Rachel L Berry Nicola J Lawrence Rachel A Ridgway Owen J Sansom Martin L Hooper

BACKGROUND Alterations in gene splicing occur in human sporadic colorectal cancer (CRC) and may contribute to tumour progression. The K-ras proto-oncogene encodes two splice variants, K-ras 4A and 4B, and K-ras activating mutations which jointly affect both isoforms are prevalent in CRC. Past studies have established that splicing of both the K-ras oncogene and proto-oncogene is altered in CRC ...

Journal: :Blood 1994
A Neubauer R K Dodge S L George F R Davey R T Silver C A Schiffer R J Mayer E D Ball D Wurster-Hill C D Bloomfield

Mutations of the N- and K-ras genes are the most frequent genetic aberrations in acute myeloid leukemia (AML) and their detection in preleukemic conditions such as the myelodysplastic syndrome (MDS) suggests a role in the earliest phases of leukemogenesis. Despite these observations, little is known about the clinical importance of ras mutations in AML. We studied the clinical impact of ras mut...

2010
Isabel Fuentes-Calvo Ana M. Blázquez-Medela Eugenio Santos José M. López-Novoa Carlos Martínez-Salgado

BACKGROUND Ras GTPases are considered cytoplasmic proteins that must be localized to cell membranes for activation, and there are few evidences of the presence of any Ras isoform in nuclei of eukaryotic cells. METHODOLOGY/PRINCIPAL FINDINGS Using conventional antibodies and inmunocytochemistry, differential centrifugation and western blot, we have observed the putative presence of K-Ras isofo...

Journal: :Carcinogenesis 2010
Juan F Santibanez Eduardo Pérez-Gómez Africa Fernandez-L Eva M Garrido-Martin Amancio Carnero Marcos Malumbres Calvin P H Vary Miguel Quintanilla Carmelo Bernabéu

Endoglin is a coreceptor for transforming growth factor-β (TGF-β) that acts as a suppressor of malignancy during mouse skin carcinogenesis. Because in this model system H-Ras activation drives tumor initiation and progression, we have assessed the effects of endoglin on the expression of H-Ras in transformed keratinocytes. We found that TGF-β1 increases the expression of H-Ras at both messenger...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید