GATA1 CMV Expression Vector
- Known as:
- GATA1 cytomegalovirus Expression Vector
- Catalog number:
- ME0049
- Product Quantity:
- 15 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GATA1 CMV Expression Vector
Ask about this productRelated genes to: GATA1 CMV Expression Vector
- 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
Related products to: GATA1 CMV Expression Vector
Related articles to: GATA1 CMV Expression Vector
- Congenital Dyserythropoietic Anemia type I (CDA-I) is an autosomal recessive disease characterized by anemia due to ineffective erythropoiesis and results primarily from mutations in CDAN1, which encodes CODANIN1. Research efforts to understand the CDA-I pathogenesis have been impeded by the embryonic lethality of germline Cdan1 deleted mice as well as mice deleted for Cdan1 in the erythroid compartment, using the constitutively active EpoR-Cre allele. To study the function of CODANIN1 in adult erythropoiesis, we generated mice with inducible erythroid-specific biallelic Cdan1 deletion using the Gata1-CreERT2 allele. Following tamoxifen administration to adult mice, Cdan1 is excised, resulting in features of CDA-I, including anemia, impaired erythroid differentiation, disturbances in erythroblast cell cycle progression, and the finding of 'spongy' heterochromatin in bone marrow erythroblasts. These findings confirm a critical role for CODANIN1 in effective adult erythropoiesis and demonstrate the successful generation of an inducible CDA-I mouse model, which serves as a valuable platform for testing novel therapies for this orphan disease. - Source: PubMed
Publication date: 2026/09/02
Friedman AnnKing Richard AMyers GreggoryYu LeiBergin Ingrid LLin ZesenDrysdale ClaireMullin CareaCruz Edgar DBalbin-Cuesta GinetteLiu Xiaofang LGallagher Patrick JZhu GuojingMcGee BethLang AnnemarieSingh Sharon AEngel James DouglasGallagher Patrick GKhoriaty Rami - We discovered that vitamin C import through the vitamin C transporter SLC23A2 in stress-specific erythroid progenitors represents a key regulatory nexus in the recovery of the erythron. In response to erythroid stress, such as blood loss, Epo induces the expression of Slc23a2 in stress erythroid progenitor cells, increasing intracellular vitamin C levels and promoting their differentiation into erythroblasts. Vitamin C-induced erythroid differentiation is blocked by Slc23a2 deletion or in EpoR mutant mice unable to induce Slc23a2. Both mice show attenuated erythron recovery in stress. These defects are rescued by exogenous expression of either SLC23A2 or the related vitamin C transporter SLC23A1, but not by a transport-defective SLC23A2 mutant. Mechanistically, intracellular vitamin C promotes erythroid progenitor differentiation independently of its antioxidant activity. Instead, it regulates 2-oxoglutarate-dependent dioxygenases, TET2, KDM6A and ALKBH8, facilitating the upregulation of the master erythroid transcription factor GATA1. These findings identify vitamin C uptake as an Epo-licensed, rate-limiting determinant of stress erythropoiesis. - Source: PubMed
Publication date: 2026/09/02
Hsieh Hsi-HsienMa YueDeVilbiss Andrew WComazzetto StefanoSubramaniyan IndhumathyJun Ji HyungVoit Richard ALi LiAgathocleous MichailHuang Lily Jun-Shen - Radiation-induced thrombocytopenia (RIT) is a severe, dose-limiting complication of cancer radiotherapy with limited clinical management options. This study investigated the therapeutic efficacy and molecular mechanism of Diosgenin glucoside (DG), a natural constituent uniquely prioritized through a graph-based deep learning virtual screening pipeline utilizing the directed graph intersection network (DGIN) architecture. - Source: PubMed
Publication date: 2026/09/01
Kong WeijieLi ZhichaoLiu ZhixuanWang LongLuo Jiesi - Runt-related transcription factor 1/acute myeloid leukemia 1 (RUNX1/AML1) is essential for the generation of myeloid progenitor cells and differentiation of megakaryocytes (MKs). During megakaryocyte differentiation and maturation, RUNX1 forms transcriptional complexes with transcription factors such as GATA-1, Ets-1, Fli-1, and NF-E2 to promote platelet production. Disruption of RUNX1 is implicated in hematopoietic neoplasms like familial platelet disorder (FPD/AML), myelodysplastic syndrome (MDS) and acute myeloid leukemia. Here, we review the transcriptional regulation of RUNX1 in megakaryocyte differentiation of normal individuals and myeloid leukemia patients. We also summarize post-translational modifications (PTMs) of RUNX1 and discuss their potential implications for novel RUNX1-directed leukemia therapies. - Source: PubMed
Publication date: 2026/08/24
Xie YanNg IanianLiu YuankaiWang HaitaoYang Qiong - Hematopoietic stem cells (HSCs) constitute an organized hematopoietic system that undergoes age-related alterations, including increased platelet production and decreased erythropoiesis. The fundamental mechanisms driving these shifts remain incompletely understood. We used single-cell RNA sequencing data to show that old HSCs contain two distinct transcriptional programs: one shared with megakaryocytes and the other reflecting the most primitive HSC state. Developmental time-series profiling further suggests that the acquisition of these programs begins early in life, with the primitive module rising prenatally and megakaryocytic priming emerging after birth. Using a fine-tuned Geneformer (transformer-based deep learning model) to capture higher-order differences between young and old HSCs, coupled with transcriptomic and epigenetic profiling, as well as transcription factor screens, we identified Pbx1 as a key regulator of these age-related transcriptional and differentiation changes. Specifically, Pbx1 suppresses erythroid differentiation by repressing Gata1 expression. These findings provide insight into HSC aging and may inform approaches to modulate age-associated HSC dysfunction. - Source: PubMed
Publication date: 2026/08/21
Kobayashi HiroshiWatanuki ShintaroShiozawa YusukeOshima MotohikoKoide ShuheiTakayama NaoyaMorikawa TakayukiHaraguchi MihoTamaki ShinpeiAsakura TakayoshiMiyata ToshioIwama AtsushiOgawa SeishiTakubo Keiyo