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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 Proteins) in B-ALL
Ikaros regulates expression of the BCL6 (show BCL6 Proteins)/BACH2 (show BACH2 Proteins) axis in acute lymphoblastic leukemia cells.
high CRLF2 expression works with the IKZF1 deletion to drive oncogenesis of acute lymphoblastic leukemia
expression of both CEBPE and IKZF1 in patient leukemic B cells was most similar to that in early stage B cells, believed to be the B-ALL cell-of-origin
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
We systematically screened 6 potentially functional SNPs in ARID5B and IKZF1 genes.
Two families with a Common variable immunodeficiency-like syndrome with normal hematologic parameters and fetal hemoglobulin silencing with heterozygote IKZF1 mutations.
IKZF1 rs10235796 C allele, IKZF1 rs6964969A>G, CDKN2A rs3731246 G>C, and CDKN2A rs3731246 C allele were signi fi cantly associated with Acute Lymphoblastic Leukemia in Yemenis of Arab-Asian descent. Borderline association found in IKZF1 rs4132601 T>G variant. No associations found with IKZF1 rs11978267 or rs7789635, DDC (show DDC Proteins) rs3779084; rs880028; rs7809758, CDKN2A rs3731217, CEBPE (show CEBPE Proteins) rs2239633; rs12434881
Silence of IKZF1 expression in MHCC-LM3 and MHCC-97L cell lines revealed a approximately 1.84- and approximately 2.27-fold rise in MDIG (show MINA Proteins) mRNA levels.
These data describe a novel regulatory mechanism through which STAT3 (show STAT3 Proteins) and the Ikaros zinc finger transcription factors Aiolos (show IKZF3 Proteins) and Ikaros cooperate to regulate Bcl-6 (show BCL6 Proteins) expression.
Ikaros is a transcriptional regulator required for maintaining levels of Foxo1 (show FOXO1 Proteins) gene expression in naive T-cells.
ADAMTS10 (show ADAMTS10 Proteins) is identified as a potential functional integrator of the Ikaros-CtBP (show CTBP2 Proteins) 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 Proteins).
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