Mouse Anti-IKZF1 Recombinant Antibody (CBT3783) (V2LY-0625-LY1715)

Name: Mouse Anti-IKZF1 Recombinant Antibody (CBT3783)
SKU: V2LY-0625-LY1715
Rating: 5 (1 reviews)

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Tested Data

Mouse Anti-IKZF1 Recombinant Antibody (CBT3783) (V2LY-0625-LY1715) in ELISA

Mouse Anti-IKZF1 Recombinant Antibody (CBT3783) (V2LY-0625-LY1715) in WB

Mouse Anti-IKZF1 Recombinant Antibody (CBT3783) (V2LY-0625-LY1715) in FC

Mouse Anti-IKZF1 Recombinant Antibody (CBT3783) (V2LY-0625-LY1715) in IF

Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBT3783

Application

ICC, FC

Immunogen

Purified recombinant fragment of human IKZF1 (AA: 401-520) expressed in E. Coli.

Host Species

Mouse

Specificity

Human

Antibody Isotype

IgG2b

Clonality

Monoclonal Antibody

Application Notes

Application	Note
WB	1:500-1:2,000
ICC	1:200-1:1,000
FC	1:200-1:400
ELISA	1:10,000

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

Format

Liquid

Buffer

PBS

Preservative

Sodium azide

Concentration

Batch dependent

Purity

> 95% Purity determined by SDS-PAGE.

Storage

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

More Infomation

Target

Full Name

IKAROS family zinc finger 1

Entrez Gene ID

10320

UniProt ID

Q13422

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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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
Other Protocols

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

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