Faculty Opinions recommendation of Critical requirement of VEGF-C in transition to fetal erythropoiesis.

Author(s):  
Guillermo Oliver ◽  
Wanshu Ma
Blood ◽  
2016 ◽  
Vol 128 (5) ◽  
pp. 710-720 ◽  
Author(s):  
Shentong Fang ◽  
Harri Nurmi ◽  
Krista Heinolainen ◽  
Shuo Chen ◽  
Essi Salminen ◽  
...  

Key Points Vegfc is essential for mobilization, maturation, and enucleation of primitive erythroblasts. Vegfc deletion compromises liver colonization by erythro-myeloid progenitors and subsequent macrophage/erythroid expansion.


2013 ◽  
pp. 76-81
Author(s):  
Thi Anh Thu Nguyen ◽  
Thi Mai Dung Nguyen

Background: Colorblind disability causes difficulties for people in daily life. Derived from the critical requirement to detect the patients in order to help prevent inappropriate careers, especially careers related to transportation, this research aim to determine the situations and the distributions of different types of visual disabilities. Materials: 1174 students (787 boys and 387 girls) including 2 groups: occupation group and transportation group were tested with ISHIHARA chromatic plates for colour vision deficiencies (CVD) (CVD iclude the total colour blindness, red- green blindness, red-blindness, green- blindness). The results are showed as follow: (i) Frequency of CVD boys among boy group is 4.70%; (ii) Frequency of CVD girls among girls group is 2.58%; (iii) In boy group, among 3 types of red- green blindness, the green-blindness has the higher frequency (3.18%) comparision with these ones of the red- green blindness and red-blindness. The total colour defiency was hardly; (iv) Frequency of CVD students among occupation group is 4.15%; (v) Frequency of CVD students among transportation group is 3.83%.


Blood ◽  
1978 ◽  
Vol 51 (3) ◽  
pp. 539-547 ◽  
Author(s):  
DH Chui ◽  
SK Liao ◽  
K Walker

Abstract Erythroid progenitor cells in +/+ and Sl/Sld fetal livers manifested as burst-forming units-erythroid (BFU-E) and colony-forming units- erythroid (CFU-E) were assayed in vitro during early development. The proportion of BFU-E was higher as mutant than in normal fetal livers. On the other hand, the proportion of CFU-E was less in the mutant than in the normal. These results suggest that the defect in Sl/Sld fetal hepatic erythropoiesis is expressed at the steps of differentiation that effect the transition from BFU-E to CFU-E.


Blood ◽  
2013 ◽  
Vol 122 (6) ◽  
pp. 988-998 ◽  
Author(s):  
Yehudit Birger ◽  
Liat Goldberg ◽  
Timothy M. Chlon ◽  
Benjamin Goldenson ◽  
Inna Muler ◽  
...  

Key Points Transient expansion of fetal megaerythroid progenitors in ERG/Gata1s mouse is biologically similar to Down syndrome TMD. The N-terminal domain of GATA1 and the downregulation of ERG expression are essential for normal fetal erythropoiesis.


2021 ◽  
Vol 552 ◽  
pp. 98-105
Author(s):  
Yali Li ◽  
Huayuan Tang ◽  
Fengling Chen ◽  
Jiewen Chen ◽  
Hong Wang ◽  
...  

Cell Cycle ◽  
2010 ◽  
Vol 9 (2) ◽  
pp. 371-376 ◽  
Author(s):  
Jing Zhang ◽  
Eunice Y. Lee ◽  
Yangang Liu ◽  
Seth D. Berman ◽  
Harvey F. Lodish ◽  
...  

Oncogene ◽  
2021 ◽  
Author(s):  
Rósula García-Navas ◽  
Pilar Liceras-Boillos ◽  
Carmela Gómez ◽  
Fernando C. Baltanás ◽  
Nuria Calzada ◽  
...  

AbstractSOS1 ablation causes specific defective phenotypes in MEFs including increased levels of intracellular ROS. We showed that the mitochondria-targeted antioxidant MitoTEMPO restores normal endogenous ROS levels, suggesting predominant involvement of mitochondria in generation of this defective SOS1-dependent phenotype. The absence of SOS1 caused specific alterations of mitochondrial shape, mass, and dynamics accompanied by higher percentage of dysfunctional mitochondria and lower rates of electron transport in comparison to WT or SOS2-KO counterparts. SOS1-deficient MEFs also exhibited specific alterations of respiratory complexes and their assembly into mitochondrial supercomplexes and consistently reduced rates of respiration, glycolysis, and ATP production, together with distinctive patterns of substrate preference for oxidative energy metabolism and dependence on glucose for survival. RASless cells showed defective respiratory/metabolic phenotypes reminiscent of those of SOS1-deficient MEFs, suggesting that the mitochondrial defects of these cells are mechanistically linked to the absence of SOS1-GEF activity on cellular RAS targets. Our observations provide a direct mechanistic link between SOS1 and control of cellular oxidative stress and suggest that SOS1-mediated RAS activation is required for correct mitochondrial dynamics and function.


2015 ◽  
Vol 17 (5) ◽  
pp. 1246-1254 ◽  
Author(s):  
Denison J. Kuruvilla ◽  
John A. Widness ◽  
Demet Nalbant ◽  
Robert L. Schmidt ◽  
Donald M. Mock ◽  
...  
Keyword(s):  

PLoS Biology ◽  
2007 ◽  
Vol 5 (10) ◽  
pp. e252 ◽  
Author(s):  
Merav Socolovsky ◽  
Michael Murrell ◽  
Ying Liu ◽  
Ramona Pop ◽  
Ermelinda Porpiglia ◽  
...  

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