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Human Polyclonal GFI1B Primary Antibody für WB - ABIN1881370
Rödel, Wagner, Zörnig, Niessing, Möröy: The human homologue (GFI1B) of the chicken GFI gene maps to chromosome 9q34.13-A locus frequently altered in hematopoietic diseases. in Genomics 1999
Show all 2 Pubmed References
Disruption of GFI1B non-DNA-binding zinc-finger 1 is associated with mild to moderate thrombocytopenia without alpha-granule deficiency or bleeding symptomatology, indicating that the site of GFI1B mutation has important phenotypic implications. Platelet CD34 expression appears to be a common feature of perturbed GFI1B function.
Platelet CD34 expression and alpha/delta-granule abnormalities in GFI1B- and RUNX1-related familial bleeding disorders.
GFI1B is an essential protein for the normal development of the megakaryocyte lineage
High GFI1B expression is associated with small-cell lung cancer.
Results demonstrate that alpha-delta platelet storage pool deficiency is associated with either a heterozygous mutation in GFI1B (de novo or familial) abrogating the binding of the zinc fingers with the promoter of its target genes, or by hypomorphic biallelic mutations leading to autosomal recessive inheritance.
study demonstrates the significance of Gfi1b regulated Kindlin3-Talin1 expression in driving megakaryocytic differentiation and highlights the contribution of cytoskeletal agents in the developmental progression of these platelet progenitors
Role for Alternative GFI1B Splice Variants in Human Hematopoiesis
SPI1-GFI1B transcriptional network is an important regulatory axis in acute myeloid leukemia as well as in the development of erythroid versus myelomonocytic cell fate
Gfi1b functions as a transcriptional repressor by recruiting histone-modifying enzymes to promoters and enhancers of target genes. Mutations are associated with certain bleeding disorders. Review.
a mutation in GFI1B causes a platelet disorder; GFI1B has a role a critical regulator of platelet shape, number, and function
results, supported by evidence from mouse models, identify GFI1 and GFI1B as prominent medulloblastoma oncogenes and implicate 'enhancer hijacking' as an efficient mechanism driving oncogene activation in a childhood cancer
TAL1 is involved in regulating H3K27me3 variations in collaboration with GFI1B
Silencing of both BCR-ABL siRNA and GFI1B siRNA is associated with an additive antileukemic effect against K562 cells.
Our studies show that GFI1B, in addition to being causally related to the gray platelet syndrome, is key to megakaryocyte and platelet development.
Gfi-1B p32, a Gfi-1B isoform, is essential for erythroid differentiation
GFI1B regulatory elements behave as activators and repressors, consistent with a model in which GFI1B binds to its own promoter and to the conserved non-coding elements as its levels rise.
Results reveal the presence of different protein complexes, including GATA-1 and Oct-1, involved in Gfi1b regulation.
repressing TGF-beta type III receptor (TbetaRIotaII) expression, Gfi-1B favors the Smad2/TIF1-gamma interaction downstream of TGF-beta signaling, allowing immature progenitors to differentiate toward the erythroid lineage.
HMGB2 potentiates GATA-1-dependent transcription of GFI1B by Oct-1 and thereby controls erythroid differentiation.
This zinc finger protein mediates erythroid expansion and has a role in normal erythropoiesis
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.
We conclude that Gfi1b controls major functions of megakaryocytes such as integrin-dependent cytoskeleton organization, spreading and migration through the regulation of PAK activity whereas the proplatelet formation defect in GFI1B-deficient megakaryocytes is due, at least partially, to an insufficient alpha-tubulin content.
these results identify Rgs18 as a new and crucial effector of Gfi1b that regulates downstream signaling and gene expression programs to orchestrate erythro-megakaryocytic lineage choices.
Gfi1b is a regulator of embryonic globin expression and embryonic and adult erythroid maturation.
Gfi1 and gfi1b repress rag transcription in plasmacytoid dendritic cells in vitro.
GFI1B, EVI5, MYB are additional mouse genes that cooperate with the human BCL6 gene to promote the development of lymphomas.
Gfi-1b directly regulates a wide spectrum of megakaryocytic and erythroid genes, predominantly repressing their expression.
There is direct yet differential regulation of meis1 transcription by Gfi1b in distinct hematopoietic lineages.
GFI1 and GFI1B are able to trigger, in the absence of RUNX1, the down-regulation of endothelial markers and the formation of round cells, a morphologic change characteristic of endothelial to hematopoietic transition.
Gfi family members are essential for normal B cell development and play an important role in modulating expression of the V(D)J recombinase.
The transcription factor Gfi1b defines the brush cell lineage and its progenitors, and with Hes1 and Atoh1 forms a fate-determining Notch signaling driven ternary switch in the developing intestinal epithelium.
adult mice conditionally deficient for Gfi1b show a significant expansion of functional HSCs in the bone marrow and blood
role for auto- and trans-regulation of Gfi1 by GFI1 and GFI1B in maintaining the normal expression patterns of Gfi1
Gfi1b can auto-repress its own expression, but, in addition, is also able to cross-repress expression of the Gfi1 gene.
Data show that Gfi1b can replace Gfi1 functionally in haematopoiesis but not in inner ear hair cell development, demonstrating that Gfi1 and Gfi1b have equivalent and domain-dependent, cell type-specific functions.
Results suggest that Gfi1b functions in heterochromatin formation and silencing of euchromatic transcription by recruiting histone methyl transferases to either gamma-satellite sequences or specific target gene promoters.
Gfi1b was found to be up-regulated in early stages of B-cell and in a subset of early T-cell development, where Gfi1 is also present, suggesting that cross-regulation of both loci exists but is cell-type specific
Chromatin regulatory proteins CoREST and LSD1 mediate transcriptional repression by Gfi proteins.
Essential transcriptional regulator necessary for development and differentiation of erythroid and megakaryocytic lineages. Alters histone methylation by recruiting histone methyltransferase to target genes promoters. Plays a role in heterochromatin formation.
growth factor independent 1B (potential regulator of CDKN1A, translocated in CML)
, growth factor independent 1B transcription repressor
, growth factor independent protein 1B
, potential regulator of CDKN1A translocated in CML
, zinc finger protein Gfi-1b
, growth factor-independent protein 1B
, zinc finger protein 544
, growth factor independent 1B-like protein
, Zinc finger protein Gfi-1b