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Mouse Anti-HDAC7 Recombinant Antibody (CBFYH-0888) (CBMAB-H1816-FY)

This product is mouse antibody that recognizes HDAC7. The antibody CBFYH-0888 can be used for immunoassay techniques such as: WB, ELISA.
See all HDAC7 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYH-0888
Antibody Isotype
IgG2b
Application
WB, ELISA

Basic Information

Specificity
Human
Antibody Isotype
IgG2b
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
Concentration
0.4 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Histone Deacetylase 7
Introduction
Histones play a critical role in transcriptional regulation, cell cycle progression, and developmental events. Histone acetylation/deacetylation alters chromosome structure and affects transcription factor access to DNA. The protein encoded by this gene has sequence homology to members of the histone deacetylase family. This gene is orthologous to mouse HDAC7 gene whose protein promotes repression mediated via the transcriptional corepressor SMRT. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
Entrez Gene ID
UniProt ID
Alternative Names
Histone Deacetylase 7; Histone Deacetylase 7A; EC 3.5.1.98; HDAC7A; HD7A; HD7
Function
Responsible for the deacetylation of lysine residues on the N-terminal part of the core histones (H2A, H2B, H3 and H4). Histone deacetylation gives a tag for epigenetic repression and plays an important role in transcriptional regulation, cell cycle progression and developmental events. Histone deacetylases act via the formation of large multiprotein complexes. Involved in muscle maturation by repressing transcription of myocyte enhancer factors such as MEF2A, MEF2B and MEF2C. During muscle differentiation, it shuttles into the cytoplasm, allowing the expression of myocyte enhancer factors (By similarity).

May be involved in Epstein-Barr virus (EBV) latency, possibly by repressing the viral BZLF1 gene. Positively regulates the transcriptional repressor activity of FOXP3 (PubMed:17360565).

Serves as a corepressor of RARA, causing its deacetylation and inhibition of RARE DNA element binding (PubMed:28167758).

In association with RARA, plays a role in the repression of microRNA-10a and thereby in the inflammatory response (PubMed:28167758).
Biological Process
Cell-cell junction assembly Source: Ensembl
Chromatin organization Source: UniProtKB-KW
Negative regulation of interleukin-2 production Source: BHF-UCL
Negative regulation of NIK/NF-kappaB signaling Source: UniProtKB
Negative regulation of osteoblast differentiation Source: UniProtKB
Negative regulation of transcription by RNA polymerase II Source: Ensembl
Positive regulation of cell migration involved in sprouting angiogenesis Source: BHF-UCL
Protein deacetylation Source: UniProtKB
Vasculogenesis Source: Ensembl
Cellular Location
Nucleus; Cytoplasm. In the nucleus, it associates with distinct subnuclear dot-like structures. Shuttles between the nucleus and the cytoplasm. Treatment with EDN1 results in shuttling from the nucleus to the perinuclear region. The export to cytoplasm depends on the interaction with the 14-3-3 protein YWHAE and is due to its phosphorylation.
PTM
May be phosphorylated by CaMK1. Phosphorylated by the PKC kinases PKN1 and PKN2, impairing nuclear import. Phosphorylation at Ser-155 by MARK2, MARK3 and PRKD1 promotes interaction with 14-3-3 proteins and export from the nucleus. Phosphorylation at Ser-155 is a prerequisite for phosphorylation at Ser-181.

Ramnath, D., Das Gupta, K., Wang, Y., Abrol, R., Curson, J. E., Lim, J., ... & Sweet, M. J. (2022). The histone deacetylase Hdac7 supports LPS-inducible glycolysis and Il-1β production in murine macrophages via distinct mechanisms. Journal of Leukocyte Biology, 111(2), 327-336.

Xu, C., Sun, W., Liu, J., Pu, H., & Li, Y. (2022). MiR-342-3p inhibits LCSC oncogenicity and cell stemness through HDAC7/PTEN axis. Inflammation Research, 1-11.

Guo, K., Ma, Z., Zhang, Y., Han, L., Shao, C., Feng, Y., ... & Yan, X. (2022). HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway. Journal of Experimental & Clinical Cancer Research, 41(1), 91.

Axisa, P. P., Yoshida, T. M., Lucca, L. E., Kasler, H. G., Lincoln, M. R., Pham, G. H., ... & Hafler, D. A. (2022). A multiple sclerosis–protective coding variant reveals an essential role for HDAC7 in regulatory T cells. Science Translational Medicine, 14(675), eabl3651.

Ye, J., Zhong, S., Deng, Y., Yao, X., Liu, Q., Wang, J. Z., & Xiao, S. (2022). HDAC7 Activates IKK/NF-κB Signaling to Regulate Astrocyte-Mediated Inflammation. Molecular Neurobiology, 59(10), 6141-6157.

Ma, Z. Q., Feng, Y. T., Guo, K., Liu, D., Shao, C. J., Pan, M. H., ... & Hu, Y. (2022). Melatonin inhibits ESCC tumor growth by mitigating the HDAC7/β-catenin/c-Myc positive feedback loop and suppressing the USP10-maintained HDAC7 protein stability. Military Medical Research, 9(1), 54.

Hsu, A., Duan, Q., McMahon, S., Huang, Y., Wood, S. A., Gray, N. S., ... & Haldar, S. M. (2020). Salt-inducible kinase 1 maintains HDAC7 stability to promote pathologic cardiac remodeling. The Journal of clinical investigation, 130(6), 2966-2977.

Wang, R., Zhang, H., Ding, W., Fan, Z., Ji, B., Ding, C., ... & Tang, H. (2020). miR-143 promotes angiogenesis and osteoblast differentiation by targeting HDAC7. Cell Death & Disease, 11(3), 179.

Caslini, C., Hong, S., Ban, Y. J., Chen, X. S., & Ince, T. A. (2019). HDAC7 regulates histone 3 lysine 27 acetylation and transcriptional activity at super-enhancer-associated genes in breast cancer stem cells. Oncogene, 38(39), 6599-6614.

Daneshpajooh, M., Eliasson, L., Bacos, K., & Ling, C. (2018). MC1568 improves insulin secretion in islets from type 2 diabetes patients and rescues β-cell dysfunction caused by Hdac7 upregulation. Acta diabetologica, 55, 1231-1235.

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

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