نتایج جستجو برای: aptx gene

تعداد نتایج: 1141372  

2015
Jean Carroll Tristan K.W. Page Shih-Chieh Chiang Bernadett Kalmar David Bode Linda Greensmith Peter J Mckinnon Julian R. Thorpe Majid Hafezparast Sherif F. El-Khamisy

Aprataxin (APTX) deficiency causes progressive cerebellar degeneration, ataxia and oculomotor apraxia in man. Cell free assays and crystal structure studies demonstrate a role for APTX in resolving 5'-adenylated nucleic acid breaks, however, APTX function in vertebrates remains unclear due to the lack of an appropriate model system. Here, we generated a murine model in which a pathogenic mutant...

Journal: :Blood 2008
Mitch Raponi Jeffrey E Lancet Hongtao Fan Lesley Dossey Grace Lee Ivana Gojo Eric J Feldman Jason Gotlib Lawrence E Morris Peter L Greenberg John J Wright Jean-Luc Harousseau Bob Löwenberg Richard M Stone Peter De Porre Yixin Wang Judith E Karp

At present, there is no method available to predict response to farnesyltransferase inhibitors (FTIs). We analyzed gene expression profiles from the bone marrow of patients from a phase 2 study of the FTI tipifarnib in older adults with previously untreated acute myeloid leukemia (AML). The RASGRP1/APTX gene expression ratio was found to predict response to tipifarnib with the greatest accuracy...

Journal: :Human molecular genetics 2004
Nuri Gueven Olivier J Becherel Amanda W Kijas Philip Chen Orla Howe Jeanette H Rudolph Richard Gatti Hidetoshi Date Osamu Onodera Gisela Taucher-Scholz Martin F Lavin

Ataxia-oculomotor apraxia (AOA1) is a neurological disorder with symptoms that overlap those of ataxia-telangiectasia, a syndrome characterized by abnormal responses to double-strand DNA breaks and genome instability. The gene mutated in AOA1, APTX, is predicted to code for a protein called aprataxin that contains domains of homology with proteins involved in DNA damage signalling and repair. W...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2006
Makito Hirano Yoshiko Furiya Hirohide Asai Akira Yasui Satoshi Ueno

Triple A syndrome is an autosomal recessive neuroendocrinological disease caused by mutations in a gene that encodes 546 amino acid residues. The encoded protein is the nucleoporin ALADIN, a component of nuclear pore complex (NPC). We identified a mutant ALADIN(I482S) that fails to target NPC and investigated the consequences of mistargeting using cultured fibroblasts (I482Sf) from a patient wi...

Journal: :Human molecular genetics 2015
Beatriz Garcia-Diaz Emanuele Barca Andrea Balreira Luis C Lopez Saba Tadesse Sindhu Krishna Ali Naini Caterina Mariotti Barbara Castellotti Catarina M Quinzii

Ataxia oculomotor apraxia type 1 (AOA1) is an autosomal recessive disease caused by mutations in APTX, which encodes the DNA strand-break repair protein aprataxin (APTX). CoQ10 deficiency has been identified in fibroblasts and muscle of AOA1 patients carrying the common W279X mutation, and aprataxin has been localized to mitochondria in neuroblastoma cells, where it enhances preservation of mit...

Journal: :The Quarterly journal of experimental psychology. A, Human experimental psychology 1998
V Moore T Valentine

Three experiments examined whether famous faces would be affected by the age at which knowledge of the face was first acquired (AoA). Using a multiple regression design, Experiment 1 showed that rated familiarity and AoA were significant predictors of the time required to name pictures of celebrities' faces and the accuracy of producing their names. Experiment 2 replicated an effect of AoA usin...

Journal: :Blood 2012
Judith E Karp Tatiana I Vener Mitch Raponi Ellen K Ritchie B Douglas Smith Steven D Gore Lawrence E Morris Eric J Feldman Jacqueline M Greer Sami Malek Hetty E Carraway Valerie Ironside Steven Galkin Mark J Levis Michael A McDevitt Gail R Roboz Christopher D Gocke Carlo Derecho John Palma Yixin Wang Scott H Kaufmann John J Wright Elizabeth Garret-Mayer

Tipifarnib (T) exhibits modest activity in elderly adults with newly diagnosed acute myelogenous leukemia (AML). Based on preclinical synergy, a phase 1 trial of T plus etoposide (E) yielded 25% complete remission (CR). We selected 2 comparable dose levels for a randomized phase 2 trial in 84 adults (age range, 70-90 years; median, 76 years) who were not candidates for conventional chemotherapy...

2017
Parvaneh KARIMZADEH Simin KHAYATZADEH KAKHKI Shaghayegh Sadat ESMAIL NEJAD Masood HOUSHMAND Mohammad GHOFRANI

Although AOA1 (ataxia oculomotor apraxia1) is one of the most common causes of autosomal recessive cerebellar ataxias in Japanese population, it is reported from all over the world. The clinical manifestations are similar to ataxia telangiectasia in which non-neurological manifestations are absent and include almost 10% of autosomal recessive cerebellar ataxias. Dysarthria and gait disorder are...

Journal: :Blood 2012
Georgia B Vogelsang

expression to predict the clinical response to tipifarnib and etoposide. RASGRP1 is a guanine nucleotide exchange factor (GEF) that specifically activates RAS, and Aprataxin is a member of the histine triad family of nucleotide hydrolsases involved in the repair of DNA strand breaks. 3 The two-gene expression ratio (RASGRP1/APTX) was identified by analyzing gene expression profiles in bone marr...

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