نتایج جستجو برای: پروتئین asxl1

تعداد نتایج: 18286  

ژورنال: :فصلنامه پژوهشی خون 0
امیر ولیخانی a. valikhani مرکز تحقیقات انتقال خون ـ مؤسسه عالی آموزشی و پژوهشی طب انتقال خون میترا سادات رضایی m.s. rezaei استادیار مرکز تحقیقات ویروس شناسی ـ مؤسسه ملی تحقیقات سل و بیماری های ریوی ـ استادیار دانشگاه علوم پزشکی شهید بهشتیسازمان اصلی تایید شده: سازمان انتقال خون ایران (blood transfusion research center) مستانه علایی m. alaei استادیار مرکز تحقیقات انتقال خون ـ مؤسسه عالی آموزشی و پژوهشی طب انتقال خونسازمان اصلی تایید شده: دانشگاه علوم پزشکی شهید بهشتی (shahid beheshti university of medical sciences) بهزاد پوپک b. popak استادیار دانشگاه آزاد اسلامی تهران ـ واحد پزشکی تهرانسازمان اصلی تایید شده: سازمان انتقال خون ایران (blood transfusion research center) ناصر امیری زاده n. amirizade دانشیار مرکز تحقیقات انتقال خون ـ مؤسسه عالی آموزشی و پژوهشی طب انتقال خونسازمان اصلی تایید شده: دانشگاه آزاد اسلامی تهران مرکز (islamic azad university of tehran central) محمد حسین احمدی m.h. ahmadi مرکز تحقیقات انتقال خون ـ مؤسسه عالی آموزشی و پژوهشی طب انتقال خونسازمان اصلی تایید شده: سازمان انتقال خون ایران (blood transfusion research center)

چکیده سابقه و هدف ژن  asxl1به تازگی به عنوان ژن جهش یافته در لوسمی های میلوئیدی مطرح شده است. جهش در این ژن با حالت تهاجمی بیماری و پیامد بد بالینی همراه است و بررسی آن نتایج ارزشمندی در تعیین پیش آگهی بیماری در اختیار ما خواهد گذاشت. با توجه به این که فاکتورهای پیشگویی کننده محدودی برای تعیین پیش آگهی بیماران cml وجود دارد و از سویی مطالعه این ژن در بیماران ایرانی تاکنون صورت نگرفته، در این مط...

Journal: :Blood 2014
Jiapeng Wang Zhaomin Li Yongzheng He Feng Pan Shi Chen Steven Rhodes Lihn Nguyen Jin Yuan Li Jiang Xianlin Yang Ophelia Weeks Ziyue Liu Jiehao Zhou Hongyu Ni Chen-Leng Cai Mingjiang Xu Feng-Chun Yang

ASXL1 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies, and its alterations are associated with poor prognosis. De novo ASXL1 mutations cause Bohring-Opitz syndrome characterized by multiple congenital malformations. We show that Asxl1 deletion in mice led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality. Surviving As...

2013
Omar Abdel-Wahab Jie Gao Mazhar Adli Anwesha Dey Thomas Trimarchi Young Rock Chung Cem Kuscu Todd Hricik Delphine Ndiaye-Lobry Lindsay M. LaFave Richard Koche Alan H. Shih Olga A. Guryanova Eunhee Kim Sheng Li Suveg Pandey Joseph Y. Shin Leon Telis Jinfeng Liu Parva K. Bhatt Sebastien Monette Xinyang Zhao Christopher E. Mason Christopher Y. Park Bradley E. Bernstein Iannis Aifantis Ross L. Levine

Somatic Addition of Sex Combs Like 1 (ASXL1) mutations occur in 10-30% of patients with myeloid malignancies, most commonly in myelodysplastic syndromes (MDSs), and are associated with adverse outcome. Germline ASXL1 mutations occur in patients with Bohring-Opitz syndrome. Here, we show that constitutive loss of Asxl1 results in developmental abnormalities, including anophthalmia, microcephaly,...

2017
Zhaomin Li Peng Zhang Aimin Yan Zhengyu Guo Yuguang Ban Jin Li Shi Chen Hui Yang Yongzheng He Jianping Li Ying Guo Wen Zhang Ehsan Hajiramezanali Huangda An Darlene Fajardo J William Harbour Yijun Ruan Stephen D Nimer Peng Yu Xi Chen Mingjiang Xu Feng-Chun Yang

ASXL1 is frequently mutated in a spectrum of myeloid malignancies with poor prognosis. Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice; however, the underlying molecular mechanisms remain unclear. We report that ASXL1 interacts with the cohesin complex, which has been shown to guide sister chromatid segregation and regulate gene expression. Loss of Asxl1 impairs the cohesin...

2016
Hui Shi Shohei Yamamoto Mengyao Sheng Jie Bai Peng Zhang Runze Chen Shi Chen Lihong Shi Omar Abdel-Wahab Mingjiang Xu Yuan Zhou Feng-Chun Yang

ASXL1 mutations are found in a spectrum of myeloid malignancies with poor prognosis. Recently, we reported that Asxl1(+/-) mice develop myelodysplastic syndrome (MDS) or MDS and myeloproliferative neoplasms (MPN) overlapping diseases (MDS/MPN). Although defective erythroid maturation and anemia are associated with the prognosis of patients with MDS or MDS/MPN, the role of ASXL1 in erythropoiesi...

2018
Zhi-Jie Wu Xin Zhao Lauren G. Banaszak Fernanda Gutierrez-Rodrigues Keyvan Keyvanfar Shou-Guo Gao Diego Quinones Raffo Sachiko Kajigaya Neal S. Young

Additional sex combs-like 1 (ASXL1) is a well‑known tumor suppressor gene and epigenetic modifier. ASXL1 mutations are frequent in myeloid malignances; these mutations are risk factors for the development of myelodysplasia and also appear as small clones during normal aging. ASXL1 appears to act as an epigenetic regulator of cell survival and myeloid differentiation; however, the molecular mech...

2015
Ipek Yonal-Hindilerden Aynur Daglar-Aday Basak Akadam-Teker Ceylan Yilmaz Meliha Nalcaci Akif Selim Yavuz Deniz Sargin

BACKGROUND Despite insights into the genetic basis of Philadelphia-negative myeloproliferative neoplasms (Ph-negative MPNs), a significant proportion of essential thrombocythemia (ET) and primary myelofibrosis (PMF) patients present with no known MPN disease alleles. There were no previous studies investigating the impact of ASXL1 mutations in Ph-negative MPNs in Turkey. In the current study, w...

2015
Anand Balasubramani Antti Larjo Jed A. Bassein Xing Chang Ryan B. Hastie Susan M. Togher Harri Lähdesmäki Anjana Rao

ASXL1 is the obligate regulatory subunit of a deubiquitinase complex whose catalytic subunit is BAP1. Heterozygous mutations of ASXL1 that result in premature truncations are frequent in myeloid leukemias and Bohring-Opitz syndrome. Here we demonstrate that ASXL1 truncations confer enhanced activity on the ASXL1-BAP1 complex. Stable expression of truncated, hyperactive ASXL1-BAP1 complexes in a...

Journal: :Haematologica 2012
Marta Pratcorona Saman Abbas Mathijs A Sanders Jasper E Koenders François G Kavelaars Claudia A J Erpelinck-Verschueren Annelieke Zeilemakers Bob Löwenberg Peter J M Valk

Somatic mutations in the additional sex comb-like 1 (ASXL1) gene have been described in various types of myeloid malignancies, including acute myeloid leukemia. Analysis of novel markers, such as ASXL1 mutations, in independent clinical trials is indispensable before considering them for clinical decision-making. We analyzed 882 well-characterized acute myeloid leukemia cases to determine the p...

Journal: :Haematologica 2011
Brady L Stein Donna M Williams Christine O'Keefe Ophelia Rogers Roxann G Ingersoll Jerry L Spivak Amit Verma Jarek P Maciejewski Michael A McDevitt Alison R Moliterno

BACKGROUND The myeloproliferative neoplasms, essential thrombocytosis, polycythemia vera and primary myelofibrosis, share the same acquired genetic lesion, but the concept of JAK2 V617F serving as the sole lesion responsible for these neoplasms is under question, and there has been interest in identifying additional mutations that may contribute to disease pathogenesis. Because ASXL1 lesions ha...

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