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Ypel4-null Mice Display Secondary Polycythemia Associated with Ovalocytosis and Lower Band 3 Protein Levels on Red Blood Cells

ABSTRACT: Ypel4-null Mice Display Secondary Polycythemia Associated with Ovalocytosis and Lower Band 3 Protein Levels on Red Blood Cells

PROVIDER: PRJNA721452 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14218183.fastq.gz	Fastqsanger.gz
	SRR14218184.fastq.gz	Fastqsanger.gz
	SRR14218185.fastq.gz	Fastqsanger.gz
	SRR14218186.fastq.gz	Fastqsanger.gz
	SRR14218187.fastq.gz	Fastqsanger.gz

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Ypel4-null Mice Display Secondary Polycythemia Associated with Ovalocytosis and Lower Band 3 Protein Levels on Red Blood Cells

Project description:The YPEL family genes are highly conserved across a diverse range of eukaryotic organisms and thus potentially involved in essential cellular processes. Ypel4, one of five YPEL family gene orthologs in mouse and human, is highly and specifically expressed in late terminal erythroid differentiation. In this study, we investigated the role of Ypel4 in murine erythropoiesis, providing for the first time an in-depth description of a Ypel4-null phenotype in vivo. We demonstrated that the Ypel4-null mice displayed a secondary polycythemia with macro- and reticulocytosis. While lack of Ypel4 did not affect steady-state erythropoiesis in the bone marrow or spleen, the anemia-recovering capacity of Ypel4-null cells was diminished. Furthermore, Ypel4-null red blood cells (RBC) were cleared from the circulation at an increased rate, demonstrating an intrinsic defect of RBCs. Scanning electron micrographs revealed an ovalocytic morphology of Ypel4-null RBCs and functional testing confirmed reduced deformability. Even though Band 3 protein levels were shown to be reduced in Ypel4-null RBC membranes, we could not find support for a physical interaction between YPEL4 and the Band 3 protein. In conclusion, our findings provide crucial insights into the role of Ypel4 in preserving normal red cell membrane functionality.

2021-08-11 | GSE171959 | GEO

Metformin targets mitochondrial complex I to lower blood glucose levels

Project description:Metformin is among the most prescribed anti-diabetic drugs, but the primary molecular mechanism by which metformin lowers blood glucose levels is unknown. Previous studies have proposed numerous mechanisms by which acute metformin lowers blood glucose, including the inhibition of mitochondrial complex I of the electron transport chain (ETC). Here, we used transgenic mice that globally express the Saccharomyces cerevisiae protein NDI1 to determine whether the glucose lowering effect of acute oral administration of metformin requires inhibition of mitochondrial complex I of the ETC in vivo. NDI1 is a yeast NADH dehydrogenase enzyme that complements the loss of mammalian mitochondrial complex I electron transport function and is insensitive to pharmacologic mitochondrial complex I inhibitors including metformin. We demonstrate that NDI1 expression attenuates metformin’s ability to lower blood glucose levels under standard chow and high-fat diet conditions. Our results indicate that acute oral administration of metformin targets mitochondrial complex I to lower blood glucose.

2024-10-12 | GSE278099 | GEO

Investigating the proteome of red blood cells and reticulocytes in Polycythemia Vera and Essential Thrombocythemia

Project description:The project aims at comparing the effect of the JAK2V617F mutation on protein expression in human erythroid cells in the context of Polycythemia Vera and Essential Thrombocythemia

2022-02-17 | PXD029965 | Pride

Translin KO mice display elevated adiposity

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Cpd-1 null mice display a subtle neurological phenotype.

Project description:CPD1 (also known as ANP32-E) belongs to a family of evolutionarily conserved acidic proteins with leucine rich repeats implicated in a variety of cellular processes regulating gene expression, vesicular trafficking, intracellular signaling and apoptosis. Because of its spatiotemporal expression pattern, CPD1 has been proposed to play an important role in brain morphogenesis and synaptic development.We have generated CPD1 knock-out mice that we have subsequently characterized. These mice are viable and fertile. However, they display a subtle neurological clasping phenotype and mild motor deficits.CPD1 is not essential for normal development; however, it appears to play a role in the regulation of fine motor functions. The minimal phenotype suggests compensatory biological mechanisms.

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Anergic CD8+ T cells with lower levels of IL-7 receptor α

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Transcriptional cofactors display core promoter class-specificity

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Chlamydia psittaci strain:Ho Re lower

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KLF1-null neonates display hydrops fetalis and a deranged erythroid transcriptome.

Project description:We describe a case of severe neonatal anemia with kernicterus caused by compound heterozygosity for null mutations in KLF1, each inherited from asymptomatic parents. One of the mutations is novel. This is the first described case of a KLF1-null human. The phenotype of severe nonspherocytic hemolytic anemia, jaundice, hepatosplenomegaly, and marked erythroblastosis is more severe than that present in congenital dyserythropoietic anemia type IV as a result of dominant mutations in the second zinc-finger of KLF1. There was a very high level of HbF expression into childhood (>70%), consistent with a key role for KLF1 in human hemoglobin switching. We performed RNA-seq on circulating erythroblasts and found that human KLF1 acts like mouse Klf1 to coordinate expression of many genes required to build a red cell including those encoding globins, cytoskeletal components, AHSP, heme synthesis enzymes, cell-cycle regulators, and blood group antigens. We identify novel KLF1 target genes including KIF23 and KIF11 which are required for proper cytokinesis. We also identify new roles for KLF1 in autophagy, global transcriptional control, and RNA splicing. We suggest loss of KLF1 should be considered in otherwise unexplained cases of severe neonatal NSHA or hydrops fetalis.

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