نتایج جستجو برای: fetal hemoglobin hbf

تعداد نتایج: 142698  

2012
Flávia C. Costa Halyna Fedosyuk Renee Neades Johana Bravo de Los Rios Carlos F. Barbas Kenneth R. Peterson

Sickle cell disease (SCD) and β-thalassemia patients are phenotypically normal if they carry compensatory hereditary persistence of fetal hemoglobin (HPFH) mutations that result in increased levels of fetal hemoglobin (HbF, γ-globin chains) in adulthood. Thus, research has focused on manipulating the reactivation of γ-globin gene expression during adult definitive erythropoiesis as the most pro...

Journal: :Expert opinion on biological therapy 2014
Alessia Finotti Roberto Gambari

INTRODUCTION β-thalassemias are caused by nearly 300 mutations of the β-globin gene, leading to low or absent production of adult hemoglobin. Achievements have been recently obtained on innovative therapeutic strategies for β-thalassemias, based on studies focusing on the transcriptional regulation of the γ-globin genes, epigenetic mechanisms governing erythroid differentiation, gene therapy an...

2014
Stephan Menzel Helen Rooks Diana Zelenika Siana N Mtatiro Akshala Gnanakulasekaran Emma Drasar Sharon Cox Li Liu Mariam Masood Nicholas Silver Chad Garner Nisha Vasavda Jo Howard Julie Makani Adekunle Adekile Betty Pace Tim Spector Martin Farrall Mark Lathrop Swee Lay Thein

HMIP-2 is a human quantitative trait locus affecting peripheral numbers, size and hemoglobin composition of red blood cells, with a marked effect on the persistence of the fetal form of hemoglobin, HbF, in adults. The locus consists of multiple common variants in an enhancer region for MYB (chr 6q23.3), which encodes the hematopoietic transcription factor cMYB. Studying a European population co...

2017
Cyril Cyrus Chittibabu Vatte J Francis Borgio Abdullah Al-Rubaish Shahanas Chathoth Zaki A Nasserullah Sana Al Jarrash Ahmed Sulaiman Hatem Qutub Hassan Alsaleem Alhusain J Alzahrani Martin H Steinberg Amein K Al Ali

Background and Objectives. β-Thalassemia and sickle cell disease are genetic disorders characterized by reduced and abnormal β-globin chain production, respectively. The elevation of fetal hemoglobin (HbF) can ameliorate the severity of these disorders. In sickle cell disease patients, the HbF level elevation is associated with three quantitative trait loci (QTLs), BCL11A, HBG2 promoter, and HB...

Journal: :Blood 1991
E P Economou S E Antonarakis H H Kazazian G R Serjeant G J Dover

Single nucleotide substitutions in the promoter regions of the A gamma- and G gamma-globin genes have been associated with increased fetal hemoglobin (HbF) production. We wished to determine whether these or other unrecognized substitutions in the gamma promoter regions are responsible for the 20-fold variation in HbF production in sickle cell patients or normal adults. From a random sampling o...

2009
Marco Gabbianelli Ugo Testa

In humans the switch from fetal to adult hemoglobin (HbF → HbA) takes place in the perinatal and postnatal period, determining the progressive replacement of HbF with HbA synthesis (i.e., the relative HbF content in red blood cells decreases from 80-90% to <1%). In spite of more than twenty years of intensive investigations on this classic model, the molecular mechanisms regulating the Hb switc...

Journal: :Journal of laboratory physicians 2023

Abstract Background Fetal hemoglobin (HbF) levels play significant role in lowering down the morbidity and mortality sickle cell disease (SCD) patients. Coinheritance of heme oxygenase-1 (HMOX1) rs2071746:A &gt; T polymorphism may contribute to variable HbF Indian SCD Aim Objective This study was aimed evaluate HMOX1 its impact on level Materials Methods One-hundred twenty confirmed cases 50 he...

Journal: :American journal of human genetics 2017
Diyu Chen Yangjin Zuo Xinhua Zhang Yuhua Ye Xiuqin Bao Haiyan Huang Wanicha Tepakhan Lijuan Wang Junyi Ju Guangfu Chen Mincui Zheng Dun Liu Shuodan Huang Lu Zong Changgang Li Yajun Chen Chenguang Zheng Lihong Shi Quan Zhao Qiang Wu Supan Fucharoen Cunyou Zhao Xiangmin Xu

A delayed fetal-to-adult hemoglobin (Hb) switch ameliorates the severity of β-thalassemia and sickle cell disease. The molecular mechanism underlying the epigenetic dysregulation of the switch is unclear. To explore the potential cis-variants responsible for the Hb switching, we systematically analyzed an 80-kb region spanning the β-globin cluster using capture-based next-generation sequencing ...

2014
Siana Nkya Mtatiro Tarjinder Singh Helen Rooks Josephine Mgaya Harvest Mariki Deogratius Soka Bruno Mmbando Evarist Msaki Iris Kolder Swee Lay Thein Stephan Menzel Sharon E. Cox Julie Makani Jeffrey C. Barrett

BACKGROUND Fetal hemoglobin (HbF) is an important modulator of sickle cell disease (SCD). HbF has previously been shown to be affected by variants at three loci on chromosomes 2, 6 and 11, but it is likely that additional loci remain to be discovered. METHODS AND FINDINGS We conducted a genome-wide association study (GWAS) in 1,213 SCA (HbSS/HbSβ0) patients in Tanzania. Genotyping was done wi...

2016
Mohammad Ali Jalali Far Ali Dehghani Fard Saiedeh Hajizamani Majid Mossahebi-Mohammadi Hamid Yaghooti Najmaldin Saki

BACKGROUND Efficient induction of fetal hemoglobin (HbF) is considered as an effective therapeutic approach in beta thalassemia. HbF inducer agents can induce the expression of γ-globin gene and produce high levels of HbF via different epigenetic and molecular mechanisms. Thalidomide and sodium butyrate are known as HbF inducer drugs. MATERIAL AND METHODS CD133(+) stem cells were isolated fro...

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