2. 您的位置
3. 首页
4. 会议论文
5. Generating Red Cells: Balancing Self-renewal and Differentiation

Generating Red Cells: Balancing Self-renewal and Differentiation

来源 :The 2nd International Symposium on Erythrocyte Biology(2016第 | 被引量 : 0次 | 上传用户：clarrencewarren

【摘 要】

：

Thousands of cis-elements in genomes are predicted to have vital functions.While conservation,activity in surrogate assays,polymorphisms,and disease mutations provide functional clues,deletion from en

【作 者】

：

Kyle J.Hewitt Skye McIver Koichi R.Katsumura Kirby D.Johnson Colin N.Dewey Sunduz Keles Emery H.Bresnick 

【机 构】

：

University of Wisconsin School of Medicine and Public Health, Carbone Cancer Center, Dept.of Cell an

【出 处】

：

The 2nd International Symposium on Erythrocyte Biology(2016第

【发表日期】

：

2016年10期

下载到本地 , 更方便阅读

下载此文 赞助VIP

声明 : 本文档内容版权归属内容提供方 , 如果您对本文有版权争议 , 可与客服联系进行内容授权或下架

论文部分内容阅读

　　Thousands of cis-elements in genomes are predicted to have vital functions.While conservation,activity in surrogate assays,polymorphisms,and disease mutations provide functional clues,deletion from endogenous loci constitutes the gold-standard test.

其他文献

Pomalidomide reverses gamma-globin silencing during human erythropoiesis through the transcriptional

Current therapeutic strategies for sickle cell anemia are aimed at reactivating fetal hemoglobin.Pomalidomide,a third-generation immunomodulatory drug,was proposed to induce fetal hemoglobin productio

会议

Increased hepcidin in transferrin-treated thalassemic mice correlates with increased liver BMP2 expr

Iron overload results in significant morbidity and mortality in β-thalassemic patients.Insufficient hepcidin is implicated in parenchymal iron overload in β-thalassemia and approaches to increase hepc

会议

β-thalassemiairon overloadhepcidinBMP-Smad signaling

Modeling too much or too little erythropoiesis in mouse disease models

Erythropoietin (Epo) plays a critical role in the regulation of red cell mass (RCM) according to tissue oxygen levels.Hypoxia inducible factor-2 (HIF-2) is known to be a master regulator for Epo expre

会议

Chromatin signaling in transcription and erythropoiesis

The modulation of chromatin structure is a key step in transcription regulation in mammalian cells that eventually determines lineage commitment and differentiation,but the epigenetic regulators that

会议

Translational Hematology: the role of ribosomes in bone marrow failure

More than a decade has passed since the initial identification of ribosomal protein gene mutations in patients with Diamond-Blackfan anemia (DBA),a hematologic disorder that became the founding member

会议

The Critical role of plekstrin-2 in the pathogenesis of JAKV617F-induced myeloproliferative neoplasm

V617F driver mutation of JAK2 is the leading cause of Philadelphia-chromosome negative myeloproliferative neoplasms (MPNs).Studies on the pathogenesis of JAK2V617F positive MPNs have primarily focused

会议

Mutation of a GATA1 binding site in ALAS2 intron 1 arrests erythroid development in vivo

ALAS2 encodes δ-aminolevulinate synthase,which catalyzes the rate-limiting step of heme biosynthesis in erythroid cells.ALAS2 mutations are responsible for X-linked sideroblastic anemia (XLSA),which m

会议

GATA1XLSAALAS2erythroid developmentintronic mutation

PATHOGEN INACTIVATION OF BLOOD COMPONENTS TO PREVENT TRANSFUSION TRANSMITTED INFECTIONS: EFFECTS ON

Transfusion of red blood cells (RBCs) is a critical supportive therapy for healthcare.Experience over the past 50 years has shown that infectious pathogens can enter the blood donor population undetec

会议

Actin Cytoskeleton Dynamics: new mechanisms in red blood cell function

The red blood cell (RBC) membrane is supported by a network of long spectrin tetramers that interconnect short tropomyosin-coated actin filaments to form a regular hexagonal lattice,the membrane skele

会议

Leukemia cell infiltration causes defective erythropoiesis partially through MIP-1α/CCL3

Leukemia often results in severe anemia,which may significantly contribute to patient mortality and morbidity of the patients.However,the mechanisms underlying defective erythropoiesis in leukemia hav

会议

acute myeloid leukemia (AML)defective erythropoiesisMIP-1α/CCL3