GATA1 _ GATA2 EMSA Kit
- Known as:
- GATA1 _ GATA2 EMSA Kit
- Catalog number:
- AY1094
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GATA1 _ GATA2 EMSA Kit
Ask about this productRelated genes to: GATA1 _ GATA2 EMSA Kit
- Gene:
- GATA1 NIH gene
- Name:
- GATA binding protein 1
- Previous symbol:
- GF1
- Synonyms:
- ERYF1, NFE1, GATA-1, NF-E1
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
- Gene:
- GATA2 NIH gene
- Name:
- GATA binding protein 2
- Previous symbol:
- -
- Synonyms:
- NFE1B
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-03
- Date modifiied:
- 2019-04-23
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- Generation of megakaryocytes (MKs) from stem cells in vitro to produce platelets (PLTs) is an appealing approach for providing an alternative source of PLTs. Understanding the transcriptomic characteristics of MKs in vitro is crucial for providing a theoretical foundation for producing functional MKs more efficiently in the future. - Source: PubMed
Publication date: 2026/05/02
He YanminLiang YueHe JiShen YuWu ZhipanPei ShanshanZhu Faming - GATA1 and GATA2 are zinc-finger transcription factors essential for normal hematopoiesis. As genetic testing becomes more widely integrated into clinical practice, -related disorders are increasingly recognized, making it important for clinicians to understand their diagnosis and management. - Source: PubMed
Publication date: 2026/04/24
Karr MatthewPalmisiano NeilChen Xiaoyi - Postpartum depression (PPD) is a common and serious mental disorder after childbirth, imposing a heavy burden on mothers, infants, and families. Abnormalities in the tryptophan-kynurenine (TRP-KYN) metabolic pathway are considered to be involved in its pathogenesis, but the role of quinolinic acid phosphoribosyltransferase (QPRT), a key downstream enzyme in this pathway, remains unclear. This study aims to explore the association between PPD in women undergoing cesarean section and gene polymorphisms, as well as other risk factors for PPD. - Source: PubMed
Zhao ShanshanLin GuoxinLi ZiyuanPing AnqiWang SaiyingDuan Kaiming - Erythroid differentiation requires precise regulation of transcription factor binding to chromatin targets as hematopoietic progenitors relinquish multipotency and activate lineage programs. GATA2 maintains progenitor identity and is thought to be progressively silenced as GATA1 levels rise. However, the precise changes in GATA2 chromatin binding kinetics during this transition remain undefined. Here, we combined live-cell single-molecule imaging in cell lines and primary mouse progenitors with CUT&Tag chromatin profiling to define GATA2 activity during erythropoiesis. Single-molecule tracking resolved two interaction modes: short-lived (<1 s) searching interactions and long-lived (>5 s) binding. Surprisingly, early erythroid differentiation was characterized by a transitory strengthening of long-lived GATA2 chromatin engagement. This manifested as increased residence time of GATA2 bound to chromatin in G1E-ER4 cells and an expansion of the long-lived bound population in HPC7 cells and primary mouse progenitors. This transitory phase of enhanced engagement declined upon further differentiation. Genome-wide mapping identified regulatory elements selectively occupied by GATA2 during this early transition state, revealing promoter-proximal sites enriched for GATA/RUNX motifs and distal elements containing composite GATA/E-box signatures. Together, our imaging and chromatin profiling indicate that GATA2 chromatin engagement is kinetically remodeled at the onset of differentiation, with early recruitment targets partitioning into distinct promoter- and enhancer-associated subclasses. These results support a model in which transcription factor kinetics constitute a dynamic chromatin engagement layer that characterizes the GATA2-to-GATA1 transition. - Source: PubMed
Publication date: 2026/03/06
Hobbs John WTaylor Samuel JKumari RajniHaque NayemVictor Lou LouSteidl UlrichColeman Robert A - Erythropoiesis is a highly coordinated process that generates mature red blood cells from hematopoietic stem-progenitor cells (HSPCs). Erythropoietin (EPO) is a major regulator of erythropoiesis and binds to the erythropoietin receptor (EPOR), leading to increased erythroid differentiation and proliferation. MicroRNAs (miRs) are important developmental regulators, and distinct miR expression patterns are associated with specific stages of hematopoietic differentiation. Expression profiling of EPO-stimulated human HSPCs revealed increased expression of miR-513a-5p in early erythroid cells. Enforced expression of miR-513a in primary human CD34 HSPCs promoted erythroid differentiation, as determined by cell-surface marker expression and increased levels of erythroid molecules including hemoglobin. Similar results were observed in human TF-1 erythroleukemia cells, where miR-513a stimulated erythroid differentiation including increased GATA1 and hemoglobin expression and decreased GATA2 expression, even in the absence of EPO. Notably, miR-513a promoted erythroid differentiation in EPOR knockout (KO) TF-1 cells, but not in GATA1 KO TF-1 cells, indicating that miR-513a requires GATA1, but not EPOR, to stimulate erythropoiesis. Further analysis revealed that enforced expression of miR-513a was associated with reduced c-Jun and phospho-c-Jun protein levels. Overexpression of c-Jun inhibited both EPO- and miR-513a-stimulated erythropoiesis. Conversely, c-Jun KO TF-1 cells had increased hemoglobin protein expression, even in the absence of EPO, phenocopying miR-513a overexpression. In summary, this study identifies miR-513a as a positive regulator of early human erythropoiesis and supports a role for miR-513a in promoting erythroid differentiation by modulating c-Jun expression and increasing GATA1 expression. - Source: PubMed
Publication date: 2026/03/08
Kim MinJungTaylor BrittanyBolten ShannonEberly Christian LAbdurahman MahliyaCreed T MichaelYang AcongHatchet Taylor LDyson TristanGu ShuoCivin Curt IKingsbury Tami J