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Mouse Anti-IKZF1 Recombinant Antibody (CB410A) (CBMAB-CA410LY)

The product is antibody recognizes IKZF1. The antibody CB410A immunoassay techniques such as: ELISA, WB.
See all IKZF1 antibodies

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Cattle
Clone
CB410A
Antibody Isotype
IgG1
Application
ELISA, WB

Basic Information

Immunogen
Recombinant fragment, corresponding to amino acids 249-415aa of Human IKAROS (C-terminus).
Specificity
Human, Mouse, Cattle
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
IKAROS family zinc finger 1
Introduction
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. Most isoforms share a common C-terminal domain, which contains two zinc finger motifs that are required for hetero- or homo-dimerization, and for interactions with other proteins. The isoforms, however, differ in the number of N-terminal zinc finger motifs that bind DNA and in nuclear localization signal presence, resulting in members with and without DNA-binding properties. Only a 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 are 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). [provided by RefSeq, May 2014]
Entrez Gene ID
Human10320
Mouse22778
Cattle541154
UniProt ID
HumanQ9Y6K9
MouseO88522
Alternative Names
IKAROS Family Zinc Finger 1
Function
Transcription regulator of hematopoietic cell differentiation (PubMed:17934067).

Binds gamma-satellite DNA (PubMed:17135265, PubMed:19141594).

Plays a role in the development of lymphocytes, B- and T-cells. Binds and activates the enhancer (delta-A element) of the CD3-delta gene. Repressor of the TDT (fikzfterminal deoxynucleotidyltransferase) gene during thymocyte differentiation. Regulates transcription through association with both HDAC-dependent and HDAC-independent complexes. Targets the 2 chromatin-remodeling complexes, NuRD and BAF (SWI/SNF), in a single complex (PYR complex), to the beta-globin locus in adult erythrocytes. Increases normal apoptosis in adult erythroid cells. Confers early temporal competence to retinal progenitor cells (RPCs) (By similarity).

Function is isoform-specific and is modulated by dominant-negative inactive isoforms (PubMed:17135265, PubMed:17934067).
Biological Process
Cell cycle Source: UniProtKB-KW
Chromatin organization Source: UniProtKB-KW
Erythrocyte differentiation Source: UniProtKB
Lymphocyte differentiation Source: UniProtKB
Mesoderm development Source: ProtInc
Negative regulation of transcription, DNA-templated Source: UniProtKB
Regulation of transcription by RNA polymerase II Source: GO_Central
Cellular Location
Nucleus. In resting lymphocytes, distributed diffusely throughout the nucleus. Localizes to pericentromeric heterochromatin in proliferating cells. This localization requires DNA binding which is regulated by phosphorylation / dephosphorylation events.
Isoform Ik2: Nucleus. In resting lymphocytes, distributed diffusely throughout the nucleus. Localizes to pericentromeric heterochromatin in proliferating cells. This localization requires DNA binding which is regulated by phosphorylation / dephosphorylation events (By similarity).
Isoform Ik6: Cytoplasm
Involvement in disease
Defects in IKZF1 are frequent occurrences (28.6%) in acute lymphoblasic leukemia (ALL). Such alterations or deletions lead to poor prognosis for ALL.
Chromosomal aberrations involving IKZF1 are a cause of B-cell non-Hodgkin lymphomas (B-cell NHL). Translocation t(3;7)(q27;p12), with BCL6.
Immunodeficiency, common variable, 13 (CVID13):
A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. CVID13 is an autosomal dominant disease associated with a striking decrease in B-cell numbers.
PTM
Phosphorylation controls cell-cycle progression from late G1 stage to S stage. Hyperphosphorylated during G2/M phase. Dephosphorylated state during late G1 phase. Phosphorylation on Thr-140 is required for DNA and pericentromeric location during mitosis. CK2 is the main kinase, in vitro. GSK3 and CDK may also contribute to phosphorylation of the C-terminal serine and threonine residues. Phosphorylation on these C-terminal residues reduces the DNA-binding ability. Phosphorylation/dephosphorylation events on Ser-13 and Ser-295 regulate TDT expression during thymocyte differentiation. Dephosphorylation by protein phosphatase 1 regulates stability and pericentromeric heterochromatin location. Phosphorylated in both lymphoid and non-lymphoid tissues (By similarity). Phosphorylation at Ser-361 and Ser-364 downstream of SYK induces nuclear translocation.
Sumoylated. Simultaneous sumoylation on the 2 sites results in a loss of both HDAC-dependent and HDAC-independent repression. Has no effect on pericentromeric heterochromatin location. Desumoylated by SENP1 (By similarity).
Polyubiquitinated.

Hoshino, A., Boutboul, D., Zhang, Y., Kuehn, H. S., Hadjadj, J., Özdemir, N., ... & Latour, S. (2022). Gain-of-function IKZF1 variants in humans cause immune dysregulation associated with abnormal T/B cell late differentiation. Science Immunology, 7(69), eabi7160.

Mangum, D. S., Meyer, J. A., Mason, C. C., Shams, S., Maese, L. D., Gardiner, J. D., ... & Schiffman, J. D. (2021). Association of combined focal 22q11. 22 deletion and IKZF1 alterations with outcomes in childhood acute lymphoblastic leukemia. JAMA oncology, 7(10), 1521-1528.

Barrio, S., Munawar, U., Zhu, Y. X., Giesen, N., Shi, C. X., Da Viá, M., ... & Kortüm, K. M. (2020). IKZF1/3 and CRL4CRBN E3 ubiquitin ligase mutations and resistance to immunomodulatory drugs in multiple myeloma. Haematologica, 105(5), e237.

Stanulla, M., Cavé, H., & Moorman, A. V. (2020). IKZF1 deletions in pediatric acute lymphoblastic leukemia: still a poor prognostic marker?. Blood, The Journal of the American Society of Hematology, 135(4), 252-260.

Vairy, S., & Tran, T. H. (2020). IKZF1 alterations in acute lymphoblastic leukemia: The good, the bad and the ugly. Blood Reviews, 44, 100677.

Churchman, M. L., Qian, M., Te Kronnie, G., Zhang, R., Yang, W., Zhang, H., ... & Mullighan, C. G. (2018). Germline genetic IKZF1 variation and predisposition to childhood acute lymphoblastic leukemia. Cancer cell, 33(5), 937-948.

Stanulla, M., Dagdan, E., Zaliova, M., Bourquin, J. P., & Bornhauser, B. (2018). IKZF1 defines a new minimal residual disease-dependent very-poor prognostic profile in pediatric B-cell precursor acute lymphoblastic leukemia. Journal of Clinical Oncology, 36(12), 1240-1249.

Marke, R., van Leeuwen, F. N., & Scheijen, B. (2018). The many faces of IKZF1 in B-cell precursor acute lymphoblastic leukemia. haematologica, 103(4), 565.

Yeoh, A. E. J., Lu, Y., Chin, W. H. N., Chiew, E. K. H., Lim, E. H., Li, Z., ... & Ariffin, H. (2018). Intensifying treatment of childhood B-lymphoblastic leukemia with IKZF1 deletion reduces relapse and improves overall survival: results of Malaysia-Singapore ALL 2010 study. Journal of Clinical Oncology, 36(26), 2726-2735.

Boutboul, D., Kuehn, H. S., Van de Wyngaert, Z., Niemela, J. E., Callebaut, I., Stoddard, J., ... & Rosenzweig, S. D. (2018). Dominant-negative IKZF1 mutations cause a T, B, and myeloid cell combined immunodeficiency. The Journal of clinical investigation, 128(7), 3071-3087.

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For research use only. Not intended for any clinical use.

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