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Human Polyclonal GATA1 Primary Antibody für IHC - ABIN966189
Zon, Tsai, Burgess, Matsudaira, Bruns, Orkin: The major human erythroid DNA-binding protein (GF-1): primary sequence and localization of the gene to the X chromosome. in Proceedings of the National Academy of Sciences of the United States of America 1990
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Human Monoclonal GATA1 Primary Antibody für ELISA, WB - ABIN969165
Blackford, Parmigiani, Kensler, Wolfgang, Jones, Zhang, Parsons, Lin, Leary, Eshleman, Goggins, Jaffee, Iacobuzio-Donahue, Maitra, Klein, Cameron, Olino, Schulick, Winter, Vogelstein, Velculescu, Kinzler, Hruban: Genetic mutations associated with cigarette smoking in pancreatic cancer. in Cancer research 2009
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Human Monoclonal GATA1 Primary Antibody für ICC, IHC - ABIN969166
Wierenga, Vellenga, Schuringa: Down-regulation of GATA1 uncouples STAT5-induced erythroid differentiation from stem/progenitor cell proliferation. in Blood 2010
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Human Monoclonal GATA1 Primary Antibody für ELISA, WB - ABIN966186
Yerges, Klei, Cauley, Roeder, Kammerer, Moffett, Ensrud, Nestlerode, Marshall, Hoffman, Lewis, Lang, Barrett-Connor, Ferrell, Orwoll, Zmuda: High-density association study of 383 candidate genes for volumetric BMD at the femoral neck and lumbar spine among older men. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2009
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Human Polyclonal GATA1 Primary Antibody für IHC - ABIN966190
Kadri, Maouche-Chretien, Rooke, Orkin, Romeo, Mayeux, Leboulch, Chretien: Phosphatidylinositol 3-kinase/Akt induced by erythropoietin renders the erythroid differentiation factor GATA-1 competent for TIMP-1 gene transactivation. in Molecular and cellular biology 2005
Human Polyclonal GATA1 Primary Antibody für ELISA, WB - ABIN250863
Li, Godinho, Klusmann, Garriga-Canut, Yu, Orkin: Developmental stage-selective effect of somatically mutated leukemogenic transcription factor GATA1. in Nature genetics 2005
Cow (Bovine) Polyclonal GATA1 Primary Antibody für WB - ABIN2792607
de Vooght, van Wijk, van Solinge: GATA-1 binding sites in exon 1 direct erythroid-specific transcription of PPOX. in Gene 2008
Human Polyclonal GATA1 Primary Antibody für ICC, IF - ABIN4313642
Pontén, Jirström, Uhlen: The Human Protein Atlas--a tool for pathology. in The Journal of pathology 2008
Human Monoclonal GATA1 Primary Antibody für ELISA, ICC - ABIN5683395
Åström, Hahn-Strömberg, Zetterberg, Vedin, Merup, Palmblad: X-linked thrombocytopenia with thalassemia displays bone marrow reticulin fibrosis and enhanced angiogenesis: comparisons with primary myelofibrosis. in American journal of hematology 2015
Since the first discovery of GATA1 mutations in acute megakaryocytic leukemia , the number of diseases that are associated with impaired GATA1 function has increased to include Diamond Blackfan Anemia and myeloproliferative neoplasms. With respect to the latter, we are only just now appreciating the link between enhanced JAK/STAT signaling, GATA1 deficiency and disease pathogenesis.
Reduced GATA-1 could be responsible for the upregulation of IRF-3 in lung adenocarcinoma cells through binding with a specific domain of IRF-3 promoter.
described the functional interaction between GATA1 and SEC23B genes in two patients with suspected congenital dyserythropoietic anemia type II
Here, using zebrafish, murine, and human models, the authors show that erythropoietin (EPO) signaling, together with the GATA1 transcriptional target, AKAP10, regulates heme biosynthesis during erythropoiesis at the outer mitochondrial membrane.
expression of GATA1 effectively rescued maturation of Primary myelofibrosis megakaryocytes.
GATA1 is an essential downstream target of SENP1 and that the differential expression and response of GATA1 and Bcl-xL are a key mechanism underlying chronic mountain sickness pathology.
we herein show a long-distance regulatory region with GATA1 binding sites as being a strong enhancer for NBEAL2 expression.
Single-nucleotide polymorphism in GATA1 gene is associated with non-Down syndrome transient proliferative megakaryoblastic disease.
These findings indicate that erythroid specific activator GATA-1 acts at CTCF sites around the beta-globin locus to establish tissue-specific chromatin organization.
Results show that GATA1 recognizes a single GATA motif or a composite of adjacent GATA motifs and exerts its diversified bindings. These binding configurations serve as one of the critical determinants of specific transcriptional regulation.
Acquired and inherited GATA1 mutations contribute to Diamond-Blackfan anemia, acute megakaryoblastic leukemia, transient myeloproliferative disorder, and a group of related congenital dyserythropoietic anemias with thrombocytopenia.
Our results suggest that GATAl and miR-363 were involved in the regulation of hematopoiesis via the HIF-1alpha pathway in K562 cells under hypoxic condition.
analysis of GATA1 mutations in a cohort of Malaysian children with Down syndrome-associated myeloid disorder reveals distinctive genomic events
trisomy 21 perturbed hematopoietic development through the enhanced production of early hematopoietic progenitors and the upregulation of mutated GATA1, resulting in the accelerated production of aberrantly differentiated cells.
Data show that pyruvate kinase (PK) activity was decreased in the GATA1 hemizygous state and PKLR c.1284delA variant.
GATA1 mutations were identified in consecutive Down syndrome patients with transient myeloproliferative disorder or acute leukemia.
expression of GATA1 and SET7 was upregulated and positively correlated with VEGF expression and microvessel number in 80 breast cancer patients. GATA1 and SET7 are independent poor prognostic factors in breast cancer.
Molecular cytogenetic analysis of leukemic blast cells indicated that increased blast cell status was caused by transient abnormal myelopoiesis with trisomy 21 and GATA1 mutation.
deletion of P-sel disrupted megakaryocyte/neutrophil interactions in spleen, reduced TGF-beta content, and corrected the hematopoietic stem cells distribution that in Gata1(low) mice, as in primary myelofibrosis patients, is abnormally expanded in spleen.
study provides insight into GATA1 transcriptional activity and may prove a useful resource for investigating the pathogenicity of noncoding variants in human erythroid disorders.
GATA1 interacts with the STING promoter and activates the basal transcription of the STING gene.
GATA1 may be a potential regulator of Six2-maintained population of nephron progenitor cells.
Gata1(low) mice are a bona fide model of MF, which recapitulates the hyperactivation of the TPO/MPL/JAK2 axis observed in megakaryocytes from myelofibrotic patients.
the Gata-1 gene was a T3-directly regulated gene and that TRa1PV could impair erythropoiesis via repression of the Gata-1 gene and its regulated genes. These results provide new insights into how TRa1 mutants acted to cause erythroid abnormalities in patients with mutations of the THRA gene.
Gain of function with GATA1 restores the common myeloid precursor differentiation into erythroblasts that was decreased by burn injury. There is a reciprocal relationship between myeloid-specific MafB and erythroid-specific GATA1 in these cells. MafB plays a role in dampening GATA1.
Gata1-KO(DC) DCs have reduced polysialic acid levels on their surface, which is a known determinant for the proper migration of DCs toward CCL21.
removal of the the Gata1 methylation-determining region -mediated silencing machinery is the molecular basis of the initial activation of the Gata1 gene and erythropoiesis.
findings suggest that Gata1 & PU.1 transcription factors are only executing and reinforcing lineage choice once made. These results challenge the current prevailing model of early myeloid lineage choice
GATA1 and PU.1 bind in vitro and in vivo the proximal promoter region of the RPS19 gene which is frequently mutated in Diamond-Blackfan Anemia.
TAL1 and GATA1 form a precisely organized complex at a compound motif consisting of a TG 7 or 8 bp upstream of a WGATAA motif across thousands of genomic locations
We propose that the CID-dependent dimerization system combined with the EpoR intracellular domain and the Gata1 gene regulatory region generates a novel peroral strategy for the treatment of anemia.
immunoprecipitation. Our data provide new insights into the expanded regulatory circuitry that coordinates Nanog expression.
Scrib is a novel proinflammatory regulator in endothelial cells, which maintains the protein expression of GATA-like protein-1.
Inducible Gata1 suppression expands megakaryocyte-erythroid progenitors from embryonic stem cells
By ablating TAF10 specifically in erythroid cells in vivo, observed is a differentiation block accompanied by deregulated GATA1 target genes, including Gata1 itself, suggesting functional cross talk between GATA1 and TAF10.
GATA-1 deficiency can partially rescue the trabecular bone loss observed with osteoprotegerin deficiency
the dbGATA motif has a role in the maintenance of Gata1 expression in hematopoietic progenitors
gata1 is required for early initiation of mpx expression in the intermediate cell mass, however later acts to repress the neutrophil fate
this study reveals a posttranscriptional regulatory mechanism by which RNA-binding protein Elavl1a regulates embryonic erythropoiesis by maintaining appropriate levels of gata1 expression.
eaf1 has a role in suppressing foxo3b expression to modulate transcriptional activity of gata1 and spi1 in primitive hematopoiesis
The authors show that tif1gamma modulates the erythroid versus myeloid fate outcomes from HSCs by differentially controlling the levels of gata1 and pu.1.
this study provides evidence that Foggy/Spt5 plays an important role in gata1 gene expression and erythropoiesis through its transcriptional activation domain.
These results showed that young thrombocytes have higher GATA1 promoter activity, while mature thrombocytes have more FLI1 gene promoter transcription.
ability of Gata1 to self-associate critically contributes to the autoregulation of the gata1 gene
gata1 determines myelo-erythroid progenitor cell fate in zebrfish
Gata1 plays an integral role in directing myelo-erythroid lineage fate decisions during embryogenesis.
Two conserved miRNAs, miR 144 and miR 451, emerged as direct targets of the critical hematopoietic transcription factor GATA-1.
Findings suggest that the impact of Gata1 on hematopoiesis correlates with its DNA-binding ability and that primitive hematopoiesis is more sensitive to reduction in Gata1 function than definitive hematopoiesis.
This gene encodes a protein which belongs to the GATA family of transcription factors. The protein plays an important role in erythroid development by regulating the switch of fetal hemoglobin to adult hemoglobin. Mutations in this gene have been associated with X-linked dyserythropoietic anemia and thrombocytopenia.
GATA-binding factor 1
, NF-E1 DNA-binding protein
, erythroid transcription factor
, erythroid transcription factor 1
, globin transcription factor 1
, nuclear factor, erythroid 1
, transcription factor GATA1
, GATA-binding protein 1
, GATA-binding protein 1 (globin transcription factor 1)
, GATA binding protein 1 (globin transcription factor 1)
, aspartyl/glutamyl-tRNA amidotransferase subunit A
, putative amidase
, glutamyl-tRNA amidotransferase subunit A
, hematopietic transcription factor GATA-1
, GATA 1 protein
, GATA binding protein 1
, GATA binding factor-1b
, GATA-binding factor 1-B
, transcription factor xGATA-1B
, GATA binding protein 1a
, vlad tepes
, LOW QUALITY PROTEIN: erythroid transcription factor-like
, erythroid-specific transcription factor eryf1