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functional Ikaros negatively correlated with FUT4 expression
Study identified a coding germline IKZF1 variation as a risk factor for genetic predisposition to acute lymphoblastic leukemia (ALL) and showed that the majority of variants have deleterious effects on IKAROS protein functions. Moreover, these IKZF1 variants demonstrate differences in the type and magnitude of their effects.
Combination of IKAROS family zinc finger 1 protein (IKZF1) deletion and minimal residual disease (MRD) status enable better risk stratification of patients for assignment to optimal therapeutic strategies.
The cumulative recurrence rate of the children with non-functional subtypes of IKZF1 was significantly higher than that of those with functional types of IKZF1.
heterozygous mutation decreases plasmacytoid dendritic cell numbers and expands conventional dendritic cells
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 expression, and suggest that PHF2 (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-driven T-ALL in humans
Casein kinase II, glycogen synthase kinase-3, and Ikaros mediated regulation of leukemia has been summarized. (Review)
Results found Ikaros directly binding the DNM2 promoter and suppresses DNM2 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 in B-ALL
Ikaros regulates expression of the BCL6/BACH2 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.
The results introduce Rgag4 to the repertoire of effectors serving to couple the chromatin remodeler Ikaros with the hormonal stress response.
Study results identify Ikaros as a key player in the early steps of dendritic cells development.
These data describe a novel regulatory mechanism through which STAT3 and the Ikaros zinc finger transcription factors Aiolos and Ikaros cooperate to regulate Bcl-6 expression.
Ikaros is a transcriptional regulator required for maintaining levels of Foxo1 gene expression in naive T-cells.
ADAMTS10 is identified as a potential functional integrator of the Ikaros-CtBP 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.
Ikaros functions as a guardian of B-1 lymphoid pattern, and that its absence directs the differentiation of B-1 cells into phagocytes.
Ikaros is a fundamental regulator of PRC2 function in developing T cells.
Ikaros/Ets1 binding has a role on Ikzf1 expression that is exerted at least through its promoter
deletions on chromosomes 4 and 11 affecting Cdkn2a and Ikaros are a prominent feature of young adult irradiation-induced T-cell lymphoma.. tumors arising after irradiation suffer a second hit in Pten by mis-segregation or recombination
Murine pancreatic adenocarcinoma reduces Ikaros expression and disrupts T cell homeostasis
The Ikaros family of DNA-binding proteins are critical regulators of lymphocyte differentiation. (Review)
mice with targeted deletion of the fourth DNA-binding zinc finger of the transcription factor Ikaros had increased IL-22-producing, but not IL-17-producing, CD4(+) T cells in the gut.
by repressing autocrine IL-2 production, Ikaros ensures that naive CD8(+) T cells remain dependent on licensing by APCs and CD4(+) T cells, and it may therefore act as a cell-intrinsic safeguard against inappropriate CTL differentiation
binding of Ikaros and expression of its target genes were dynamically regulated at distinct stages of early B lymphopoiesis
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