Mouse Anti-KDM5B Recombinant Antibody (1G10) (CBMAB-0100-WJ)

Name: Mouse Anti-KDM5B Recombinant Antibody (1G10)
SKU: CBMAB-0100-WJ
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

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

Basic Information

Host Animal

Mouse

Clone

1G10

Application

ELISA, IF, IHC, WB

Immunogen

Paratial recombinant protein corresponding to amino acid 231-319 from human JARID1B with GST tag.

Specificity

Human

Antibody Isotype

IgG2a, Κ

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 freeze/thaw cycles.

More Infomation

Target

Full Name

lysine demethylase 5B

Introduction

KDM5B (Lysine Demethylase 5B) encodes a lysine-specific histone demethylase that belongs to the jumonji/ARID domain-containing family of histone demethylases. Diseases associated with KDM5B include Ascending Colon Cancer and Autosomal Dominant Non-Syndromic Intellectual Disability. This protein may also play a role in genome stability and DNA repair. Alternate splicing results in multiple transcript variants. An important paralog of this gene is KDM5A.

Entrez Gene ID

10765

UniProt ID

Q9UGL1

Alternative Names

CT31; PLU1; PUT1; PLU-1; JARID1B; PPP1R98; RBP2-H1; RBBP2H1A

Function

Histone demethylase that demethylates 'Lys-4' of histone H3, thereby playing a central role in histone code (PubMed:24952722, PubMed:27214403, PubMed:28262558).
Does not demethylate histone H3 'Lys-9' or H3 'Lys-27'. Demethylates trimethylated, dimethylated and monomethylated H3 'Lys-4'. Acts as a transcriptional corepressor for FOXG1B and PAX9. Favors the proliferation of breast cancer cells by repressing tumor suppressor genes such as BRCA1 and HOXA5 (PubMed:24952722).
In contrast, may act as a tumor suppressor for melanoma. Represses the CLOCK-ARNTL/BMAL1 heterodimer-mediated transcriptional activation of the core clock component PER2 (By similarity).

Biological Process

Branching involved in mammary gland duct morphogenesisIEA:Ensembl
Cellular response to fibroblast growth factor stimulusIEA:Ensembl
Cellular response to leukemia inhibitory factorIEA:Ensembl
Chromatin remodelingManual Assertion Based On ExperimentIBA:GO_Central
Histone H3-K4 demethylationManual Assertion Based On ExperimentIDA:UniProtKB
Lens fiber cell differentiationIEA:Ensembl
Mammary duct terminal end bud growthIEA:Ensembl
Negative regulation of transcription, DNA-templatedManual Assertion Based On ExperimentIDA:GDB
Positive regulation of gene expressionIEA:Ensembl
Positive regulation of mammary gland epithelial cell proliferationIEA:Ensembl
Post-embryonic developmentIEA:Ensembl
Regulation of estradiol secretionIEA:Ensembl
Response to fungicideIEA:Ensembl
Rhythmic processIEA:UniProtKB-KW
Single fertilizationIEA:Ensembl
Uterus morphogenesisIEA:Ensembl

Cellular Location

Nucleus

Involvement in disease

Mental retardation, autosomal recessive 65 (MRT65):
A form of mental retardation, a disorder characterized by significantly below average general intellectual functioning associated with impairments in adaptive behavior and manifested during the developmental period. MRT65 patients have moderate to severe intellectual disability, developmental delay, and facial dysmorphism. Camptodactyly is present in some patients.

Harrington, J., Wheway, G., Willaime-Morawek, S., Gibson, J., & Walters, Z. S. (2022). Pathogenic KDM5B variants in the context of developmental disorders. Biochimica et Biophysica Acta (BBA)-Gene Regulatory Mechanisms, 194848.

Zhang, S. M., Cai, W. L., Liu, X., Thakral, D., Luo, J., Chan, L. H., ... & Yan, Q. (2021). KDM5B promotes immune evasion by recruiting SETDB1 to silence retroelements. Nature, 598(7882), 682-687.

Li, G., Kanagasabai, T., Lu, W., Zou, M. R., Zhang, S. M., Celada, S. I., ... & Chen, Z. (2020). KDM5B is essential for the hyperactivation of PI3K/AKT signaling in prostate tumorigenesis. Cancer research, 80(21), 4633-4643.

Fu, Y. D., Huang, M. J., Guo, J. W., You, Y. Z., Liu, H. M., Huang, L. H., & Yu, B. (2020). Targeting histone demethylase KDM5B for cancer treatment. European Journal of Medicinal Chemistry, 208, 112760.

Jose, A., Shenoy, G. G., Sunil Rodrigues, G., Kumar, N. A., Munisamy, M., Thomas, L., ... & Rao, M. (2020). Histone demethylase KDM5B as a therapeutic target for cancer therapy. Cancers, 12(8), 2121.

Xhabija, B., & Kidder, B. L. (2019, August). KDM5B is a master regulator of the H3K4-methylome in stem cells, development and cancer. In Seminars in cancer biology (Vol. 57, pp. 79-85). Academic Press.

Zhang, Z. G., Zhang, H. S., Sun, H. L., Liu, H. Y., Liu, M. Y., & Zhou, Z. (2019). KDM5B promotes breast cancer cell proliferation and migration via AMPK-mediated lipid metabolism reprogramming. Experimental Cell Research, 379(2), 182-190.

Shigekawa, Y., Hayami, S., Ueno, M., Miyamoto, A., Suzaki, N., Kawai, M., ... & Yamaue, H. (2018). Overexpression of KDM5B/JARID1B is associated with poor prognosis in hepatocellular carcinoma. Oncotarget, 9(76), 34320.

Shokri, G., Doudi, S., Fathi-Roudsari, M., Kouhkan, F., & Sanati, M. H. (2018). Targeting histone demethylases KDM5A and KDM5B in AML cancer cells: a comparative view. Leukemia research, 68, 105-111.

Lebrun, N., Mehler-Jacob, C., Poirier, K., Zordan, C., Lacombe, D., Carion, N., ... & Bienvenu, T. (2018). Novel KDM5B splice variants identified in patients with developmental disorders: Functional consequences. Gene, 679, 305-313.

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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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