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anti-Human GATA2 Antibodies:
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Cow (Bovine) Polyclonal GATA2 Primary Antibody for IHC, WB - ABIN2777458
Tsuzuki, Kitajima, Nakano, Glasow, Zelent, Enver: Cross talk between retinoic acid signaling and transcription factor GATA-2. in Molecular and cellular biology 2004
Show all 6 Pubmed References
Human Polyclonal GATA2 Primary Antibody for ICC, IF - ABIN4313645
Chiang, Wang, Fazli, Qi, Gleave, Collins, Gout, Wang: GATA2 as a potential metastasis-driving gene in prostate cancer. in Oncotarget 2014
Show all 5 Pubmed References
patients with GATA2 missense mutations have a high risk of developing leukemia and this may be prevented by early HSCT with the help of new markers
In a primary immunodeficiency and the third report of HLH in GATA2-haploinsufficiency.
clinicians should considerGATA2 deficiency in patients with myelodysplasia and long-standing Mycobacterium kansasii infection
The lack of GATA2 requirement for generation of HE and non-HE indicates the critical role of GATA2-independent pathways in specification of these two distinct endothelial lineages.
This work describes 3 families with germline GATA2 mutations in which 1 member was transplanted with hematopoietic stem cell using a mutation-positive healthy related donor resulting in donor-derived posttransplant myelodysplastic syndrome (MDS)/acute myeloid leukemia (AML), recurrent MDS/AML, or fatal infection due to impaired immune reconstitution.
identify germline GATA2 mutations have a high prevalence in older pediatric patients with monosomy 7
increasing GATA2 levels are linked to prostate cancer progression and aggressiveness
The findings suggest that abnormal clonal hematopoiesis is a common event in symptomatic germline mutated GATA2 patients with MDS and also in those with hypocellular marrows without overt morphologic evidence of dysplasia, possibly indicating a pre-MDS stage warranting close monitoring for disease progression.
A novel disease-causing synonymous exonic mutation in GATA2 affecting RNA splicing.
this report describes a patient with WILD syndrome and de novo deletion mutation in the GATA2 gene
The rs2523393 A allele creates a GATA2 binding site in a progesterone-responsive distal enhancer that loops to the HLA-F promoter.
GATA2 ZF1 mutations are associated with distinct clinico-biological features and predict better prognosis, different from ZF2 mutations, in AML patients.
GATA2 hypomorphism leads to a hyperreactive defense response to infections, and this reaction is attributed to a unique intrinsic cell defect in the regulation of myeloid expansion that increases the risk of hematological neoplasm transformation.
Timely follow-up of a GATA2 deficiency patient allows successful treatment.
Low GATA2 expression due to methylation is associated with gastric cancer.
GATA2 deficiency is an immunodeficiency and bone marrow failure disorder caused by pathogenic variants in GATA2. It is inherited in an autosomal-dominant pattern or can be due to de novo sporadic germline mutation.
These findings suggest that GATA2 deficient patients may have an increased risk of melanoma and should be observed closely for new or changing skin lesions.
Our novel finding of dynamic pulsatile expression of Gata2 suggests a highly unstable genetic state in single cells concomitant with their transition to hematopoietic fate. This reinforces the notion that threshold levels of Gata2 influence fate establishment and has implications for transcription factor-related hematologic dysfunctions.
Two GATA2 mutants (gT354M and gC373R) bound the key hematopoietic differentiation factor PU.1.
Study identifies the GATA2 transcription factor as a critical regulator of matrix stiffness induced transcriptional program in the in lymphatic endothelial cells (LECs). As opposed to the previously reported activation of GATA2 by increased mechanical stimulus upon exposure of LECs to stiff matrix or oscillatory flow, study found that GATA2 expression is increased in LECs grown on a soft matrix.
GATA2 is required for connective tissue mast cell differentiation. GATA2 and MITF regulate IgE-mediated anaphylaxis.
By regulating bone trabecularization, GATA2 expression in the osteogenic lineage may contribute to the anatomical and cellular microenvironment of the hematopoietic stem cell niche required for hematopoiesis.
Enforced expression of Gata2 in embryonic stem cells-derived hemogenic endothelial cells enhances erythroid and megakaryocyte differentiation and inhibits macrophage differentiation.
Analyses of mouse models demonstrate a cell-autonomous function of GATA2 in regulating lymphatic endothelial cell (LEC) responsiveness to VEGF-C and in controlling LEC migration and sprouting in vivo.
endothelial SENP1-mediated SUMOylation drives graft arteriosclerosis by regulating the synergistic effect of GATA2 and NF-kappaB and consequent endothelial dysfunction.
We demonstrate that overexpression of Gfi1b, c-Fos, and Gata2, previously reported to transdifferentiate fibroblasts into hematopoietic progenitors in vitro, can induce long-term HSC formation in vivo.
GATA2 could affect the function of BM-MSCs in vivo, presumably by regulating the expression of extracellular signals.
Gata2 regulates a key regulatory network of gene expression for progesterone signaling at the early pregnancy stage.
Results show that GATA2 exerts a pro-inflammatory function in injured kidney collecting duct cells, by upregulating inflammatory cytokine gene expression thereby contributes to disease progression.
Gata2 mRNA levels were almost completely rescued by expression of an erythroid lineage restricted ROSA26-promotor based GATA2 transgene
Gata2 heterozygous deletion confers selective advantage to EVI1-expressing leukemia cell expansion in recipient mice
impairment of trophoblast-specific GATA2/GATA3 function could lead to early pregnancy failure
both Gata2 and Gata3 are redundantly required for differentiation of the serotonergic and glutamatergic neurons of the dorsal raphe
Dynamically and epigenetically coordinated GATA2/ETS1SOX7 transcription factor expression is indispensable for endothelial cell differentiation.
High GATA2 expression is associated with leukemia.
results suggest that GATA2 plays an important role in cell-fate specification toward the myeloid vs T-lymphocyte lineage by regulating lineage-specific transcription factors in DC progenitors, thereby contributing to DC differentiation.
These results demonstrated that an enforced expression of Gata2 in late HECs of differentiated ESCs efficiently promotes megakaryopoiesis followed by platelet production. This study provides valuable information for ex vivo platelet production from human pluripotent stem cells in future.
we identified important roles for the GATA-2 C-ZnF in bone marrow hematopoiesis via control of c-Kit expression and HSC/HSPC survival.
Data show that transforming growth factor beta (TGFbeta)-induced changes in Gata2 transcription factor and cyclin-dependent kinase inhibitor 1C (P57) expression in hematopoietic progenitors are conveyed through Smad signaling via Smad4 protein.
Gata2 as a crucial rheostat of mesenchymal stem cell fate to control osteoblast and adipocyte lineage development.
bcar3 gene is expressed downstream of Gata2 during gastrulation, and is co-expressed with gata2 but is more broadly expressed during later development; its binding partner, bcar1 shows overlapping expression patterns
results are consistent with a model in which GATA2 contributes to inhibition of canonical Wnt signaling
these findings, strongly implicate Dlx3 in the regulation of non-neural competence, and show that GATA2 contributes to non-neural competence but is not sufficient to promote it ectopically.
Studies suggest a two-component model for the binding of CBTF with gata2 promoter, requiring both a CCAAT and A-form DNA, and the double stranded RNA binding domains (dsRBDs) of CBTF component Xilf3 must be active for both binding to the promoter.
Gata-2 is a transcriptional target downstream of BMPs within ectodermal cells, while activation of the CaM KIV signaling pathway alters GATA-2 function posttranslationally, by inhibiting its acetylation.
GATA2 and/or GATA3 are involved in the regulation of trophoblast-specific gene transcription in bovine trophoblast CT-1 cells
Our results indicate that Kzp is a critical transcriptional factor for the expression of gata2 and pu.1 to modulate primitive hematopoiesis.
Sox4b is expressed in zebrafish during pituitary development and plays a crucial role in the differentiation of thyrotrope and gonadotrope cells through induction of gata2a expression
we have identified a 224 bps cis-acting element that is sufficient to drive reporter gene expression in a manner that recapitulates hematopoietic GATA-2 expression pattern in a stable transgenic zebrafish line
gata2 down-regulation is pivotal for miR-451-driven erythroid maturation
This gene encodes a member of the GATA family of zinc-finger transcription factors that are named for the consensus nucleotide sequence they bind in the promoter regions of target genes. The encoded protein plays an essential role in regulating transcription of genes involved in the development and proliferation of hematopoietic and endocrine cell lineages. Alternative splicing results in multiple transcript variants.
endothelial transcription factor GATA-2
, GATA binding protein 2
, GATA-binding protein 2
, GATA-bindning protein 2
, transcription factor GATA-2
, GATA binding factor-2
, GATA-binding factor 2
, transcription factor xGATA-2
, transcription factor NF-E1B
, glutamyl/aspartyl-tRNA(Gln/Asp) amidotransferasesubunit A
, hypothetical protein
, protein GatA2
, GATA2 transcription factor
, endothelial transcription factor GATA-2-like