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anti-Human IKZF1 Antibodies:
anti-Rat (Rattus) IKZF1 Antibodies:
anti-Mouse (Murine) IKZF1 Antibodies:
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Human Monoclonal IKZF1 Primary Antibody for ICS, WB - ABIN2689714
Georgopoulos: Haematopoietic cell-fate decisions, chromatin regulation and ikaros. in Nature reviews. Immunology 2002
Show all 5 Pubmed References
Human Polyclonal IKZF1 Primary Antibody for ELISA, WB - ABIN314228
Mullighan, Goorha, Radtke, Miller, Coustan-Smith, Dalton, Girtman, Mathew, Ma, Pounds, Su, Pui, Relling, Evans, Shurtleff, Downing: Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia. in Nature 2007
Human Polyclonal IKZF1 Primary Antibody for CyTOF, FACS - ABIN4900336
Iempridee, Reusch, Riching, Johannsen, Dovat, Kenney, Mertz: Epstein-Barr virus utilizes Ikaros in regulating its latent-lytic switch in B cells. in Journal of virology 2014
Human Polyclonal IKZF1 Primary Antibody for FACS, IHC (p) - ABIN654180
Kuiper, Waanders, van der Velden, van Reijmersdal, Venkatachalam, Scheijen, Sonneveld, van Dongen, Veerman, van Leeuwen, van Kessel, Hoogerbrugge: IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL. in Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 2010
Show all 2 Pubmed References
Human Polyclonal IKZF1 Primary Antibody for ELISA, IHC - ABIN4324147
Loeper, Asa, Ezzat: Ikaros modulates cholesterol uptake: a link between tumor suppression and differentiation. in Cancer research 2008
Mouse (Murine) Polyclonal IKZF1 Primary Antibody for WB - ABIN2668752
Zarnegar, Rothenberg: Ikaros represses and activates PU.1 cell-type-specifically through the multifunctional Sfpi1 URE and a myeloid specific enhancer. in Oncogene 2012
Mouse (Murine) Monoclonal IKZF1 Primary Antibody for ChIPSeq, ChIP - ABIN2668828
Yeung, Chung, Guess, Bell, Leinwand: Myh7b/miR-499 gene expression is transcriptionally regulated by MRFs and Eos. in Nucleic acids research 2012
IKZF1 has a role in childhood B-cell precursor acute lymphoblastic leukemia
this study shows that alteration in Ikaros expression promotes B-1 cell differentiation into phagocytes
Our results demonstrate that the IKAROS promotes PHF2 (show PHF1 Antibodies) expression, and suggest that PHF2 (show PHF1 Antibodies) (low) expression works with the IKAROS gene deletion to drive oncogenesis of ALL
present case provides the first definitive evidence on the ability of an IKAROS heterozygous mutation to cause both immunodeficiency and NOTCH1 (show NOTCH1 Antibodies)-driven T-ALL in humans
Casein kinase II (show CSNK2A1 Antibodies), glycogen synthase kinase-3, and Ikaros mediated regulation of leukemia has been summarized. (Review)
Results found Ikaros directly binding the DNM2 (show DNM2 Antibodies) promoter and suppresses DNM2 (show DNM2 Antibodies) expression in ALL tumors and cell lines.
there is a clear distinction between loss-of-function and dominant-negative IKZF1 deletions. Affected patients should thus be monitored for minimal residual disease carefully to detect incipient relapses at an early stage and they are potential candidates for alternative or intensified treatment regimes.
IKZF1 gene deletion is associated with acute lymphoblastic leukemia.
data reveal the mechanism by which chromatin remodeling and target gene expression are regulated by Ikaros alone and in complex with HDAC1 (show HDAC1 Antibodies) in B-ALL
Ikaros regulates expression of the BCL6 (show BCL6 Antibodies)/BACH2 (show BACH2 Antibodies) axis in acute lymphoblastic leukemia cells.
we identified IKZF1 as a novel regulator of glucocorticoid -induced transcriptional responses and a critical determinant of glucocorticoid -mediated cell death in normal and leukemic B cells
These data describe a novel regulatory mechanism through which STAT3 (show STAT3 Antibodies) and the Ikaros zinc finger transcription factors Aiolos (show IKZF3 Antibodies) and Ikaros cooperate to regulate Bcl-6 (show BCL6 Antibodies) expression.
Ikaros is a transcriptional regulator required for maintaining levels of Foxo1 (show FOXO1 Antibodies) gene expression in naive T-cells.
ADAMTS10 (show ADAMTS10 Antibodies) is identified as a potential functional integrator of the Ikaros-CtBP (show CTBP2 Antibodies) chromatin remodeling network.
this study shows that ablation of Ikzf1 in RORgammat+ group 3 innate lymphoid cells results in increased expansion and cytokine production, and protection against infection and colitis
Sumoylated Ikaros is less effective than unsumoylated forms at inhibiting the expansion of murine leukemic cells, and Ikaros sumoylation is abundant in human B-cell acute lymphoblastic leukemic cells, but not in healthy peripheral blood leukocytes. Our results suggest that sumoylation may be important in modulating the tumor suppressor function of Ikaros
our results identify BTG1 as a tumor suppressor in leukemia that, when deleted, strongly enhances the risk of relapse in IKZF1-deleted B-cell precursor acute lymphoblastic leukemia, and augments the glucocorticoid resistance phenotype mediated by the loss of IKZF1 function.
These results indicate that Ikaros is required to limit B1 cell homeostasis in the adult.
These results suggest that Ikaros functions as a negative regulator of follicular B cell activation (show BLNK Antibodies).
Ikaros functions as a guardian of B-1 lymphoid pattern, and that its absence directs the differentiation of B-1 cells into phagocytes.
This gene encodes a transcription factor that belongs to the family of zinc-finger DNA binding proteins associated with chromatin remodeling. The expression of this protein is restricted to the fetal and adult hemo-lymphopoietic system, and it functions as a regulator of lymphocyte differentiation. Several alternatively spliced transcript variants encoding different isoforms have been described for this gene. All isoforms share a common C-terminal domain, which contains two zinc finger motifs that are required for hetero- or homodimerization, and for interactions with other proteins. The isoforms, however, differ in the number of N-terminal zinc finger motifs that bind DNA and contain the nuclear localization signal, resulting in members with and without DNA-binding properties. Only few isoforms contain the requisite three or more N-terminal zinc motifs that confer high affinity binding to a specific core DNA sequence element in the promoters of target genes. The non-DNA-binding isoforms are largely found in the cytoplasm, and thought to function as dominant negative factors. Overexpression of some dominant-negative isoforms have been associated with B-cell malignancies, such as acute lymphoblastic leukemia (ALL).
CLL-associated antigen KW-6
, DNA-binding protein Ikaros
, Ikaros (zinc finger protein)
, ikaros family zinc finger protein 1
, lymphoid transcription factor LyF-1
, zinc finger protein, subfamily 1A, 1 (Ikaros)
, Ikaros transcription factor
, KAROS family zinc finger 1 (Ikaros)
, IKAROS family zinc finger 1 (Ikaros)
, DNA-binding protein Ikaros-like
, zinc finger protein subfamily 1A, 1