Recombinant Human HDAC9 Protein

Beta LifeScience SKU/CAT #: BL-0234SG

Recombinant Human HDAC9 Protein

Beta LifeScience SKU/CAT #: BL-0234SG
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Product Overview

Tag GST
Host Species Human
Accession NM_058176
Synonym DKFZp779K1053; HD7; HDAC; HDAC7; HDAC7B; HDAC9B; HDAC9FL; HDRP; KIAA0744; MITR
Background HDAC9 or MITR belongs to the histone deacetylase /acuc/apha family and is a component of the histone deacetylase complex. HDAC9 gene is orthologous to the Xenopus and mouse MITR genes (MEF2-interacting transcription repressor). HDAC9 represses MEF2 activity through recruitment of multicomponent corepressor complexes that include CtBP and HDACs. HDAC9 is a calcium-sensitive transcriptional repressor of MEF2 (1). Binding of calmodulin to HDAC9 leads to its dissociation from MEF2, relieving MEF2 from the transcriptional repression. HDAC9 is a signal-responsive transcriptional repressor in mouse skeletal muscle that is downregulated upon denervation (2).
Description Recombinant human HDAC9 (548-end) was produced by baculovirus in Sf9 insect cells, fused with a GST tag at N-terminus. This protein is purified with our unique purification methods.
Source Sf9 insect cells
AA Sequence 548a.a.-end
Molecular Weight ~77 kDa
Purity For specific purity information on a given lot, see related COA.
Endotoxin < 1.0 EU per μg of the protein as determined by the LAL method
Bioactivity Active
Formulation Recombinant protein is supplied in 50mM Tris-HCl, pH 7.5, 50mM NaCl, 10mM Glutathione, 0.25mM DTT, 0.1mM EDTA, 0.1mM PMSF and 25% glycerol.
Stability The recombinant protein is stable for up to 12 months at -70°C
Usage For Research Use Only
Storage Recombinant Human HDAC9 Protein should be stored should be stored at < -70°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Target Details

Target 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. Represses MEF2-dependent transcription.; Isoform 3 lacks active site residues and therefore is catalytically inactive. Represses MEF2-dependent transcription by recruiting HDAC1 and/or HDAC3. Seems to inhibit skeletal myogenesis and to be involved in heart development. Protects neurons from apoptosis, both by inhibiting JUN phosphorylation by MAPK10 and by repressing JUN transcription via HDAC1 recruitment to JUN promoter.
Subcellular Location Nucleus.
Protein Families Histone deacetylase family, HD type 2 subfamily
Database References
Associated Diseases A chromosomal aberration involving HDAC9 is found in a family with Peters anomaly. Translocation t(1;7)(q41;p21) with TGFB2 resulting in lack of HDAC9 protein.
Tissue Specificity Broadly expressed, with highest levels in brain, heart, muscle and testis. Isoform 3 is present in human bladder carcinoma cells (at protein level).

Gene Functions References

  1. This study highlights HDAC9 as a mediator of cell invasion and angiogenesis in Triple negative breast cancer (TNBC) cells through VEGF and MAPK3 by modulating miR-206 expression and suggests that selective inhibition of HDAC9 may be an efficient route for TNBC therapy. PMID: 29936177
  2. the T allele of rs2107595 in HDAC9 increases the risk of stroke but that the G allele of rs2389995 decreases the risk of stroke in the Chinese population (Meta-Analysis) PMID: 28145521
  3. HDAC9 may be a new indicator for assessing chronic heart failure. PMID: 30074176
  4. HDAC9 may be involved in the process of diabetic nephropathy. PMID: 27633396
  5. HDAC9, in cooperation with BRG1 and MALAT1, mediates a critical epigenetic pathway responsible for vascular smooth muscle cells dysfunction. PMID: 29520069
  6. M4 macrophages are a possible source for HDAC9 and MMP12 expression in advanced human carotid plaques. PMID: 28343758
  7. HDAC9 is an important epigenetic factor regulating ox-LDL-induced endothelial cell apoptosis and inflammatory factor expression. PMID: 27100479
  8. decline in HDAC9c expression over time was accompanied by increased EZH2 expression. PMID: 27250566
  9. HDAC9 might contribute to lymphomagenesis by altering pathways involved in growth and survival, as well as modulating BCL6 activity and p53 tumor suppressor function. PMID: 27799148
  10. post-translational modification of Nkx3.2 employing HDAC9-PIASy-RNF4 axis plays a crucial role in controlling chondrocyte viability and hypertrophic maturation during skeletal development in vertebrates. PMID: 27312341
  11. Data show that the gene encoding the transcription factor SOX9 was identified by a global transcriptomic approach as an HDAC9 target gene. PMID: 26930713
  12. The minor allele A of SNP rs2107595 increased coronary artery disease risk and the severity of coronary atherosclerosis in a Chinese Han population. PMID: 27494404
  13. in leiomyosarcomas (LMS), this two-faced trait of MEF2 is relevant for tumor aggressiveness. Class IIa HDACs are overexpressed in 22% of LMS, where high levels of MEF2, HDAC4 and HDAC9 inversely correlate with overall survival. The knock out of HDAC9 suppresses the transformed phenotype of LMS cells, by restoring the transcriptional proficiency of some MEF2-target loci PMID: 28419090
  14. Based on this study, it is suggested that HDAC9 regulates the formation of APBs and could be a candidate for the target of ALT-cancer therapy. PMID: 27833022
  15. PC3/Tis21 associates with HDAC1, HDAC4, and HDAC9 in vivo, in fibroblast cells. PMID: 27333946
  16. HDAC9 is a target of miR-377 in oral squamous cell carcinoma. PMID: 28267394
  17. Studied HDAC9 gene's association with an increased susceptibility to acute coronary syndrome (ACS) in Chinese Han population. The results revealed a significant association of rs2240419 with ACS risk in which the A allele (P = 0.047) and the A allele carriers (AA + AG) (P = 0.037) were more likely to be in ACS group as compared to those in the control group. PMID: 27642596
  18. Downregulation of HDAC9 promotes gliomas. PMID: 27495233
  19. overexpression of HDAC9 contributes to OSCC carcinogenesis via targeting a transcription factor, MEF2D, and NR4A1/Nur77, a pro-apoptotic MEF2 target PMID: 26992905
  20. The aurora kinase A inhibited by MLN 8054 are both implicated in cell cycle progression and, thus, in cellular proliferation.Epigenetic regulators were targeted by SAHA inhibiting HDACs and by DZNep inhibiting the histone methyltransferase EZH2, which silences genes by trimethylating histone H3K27.Combinations of small molecular inhibitors act synergistically in rhabdoid tumor PMID: 27466490
  21. These results highlighting the significant correlation between TWIST and HDAC9 gene expression suggest that both genes may contribute to plaque stability in a coordinated way PMID: 26621503
  22. Polymorphisms of HDAC9 is associated with Ischemic Stroke. PMID: 26347468
  23. The results imply that HDAC9 is involved in the transcriptional regulation of human odontoblasts in vivo. PMID: 22297573
  24. HDAC9 was commonly expressed in retinoblastoma tissues and HDAC9 was overexpressed in prognostically poor retinoblastoma patients. PMID: 27033599
  25. HDAC9 promotes tumor formation of glioblastoma via TAZ-mediated EGFR pathway activation. PMID: 25760078
  26. the results of this study suggest that targeting HDACs by ST-3595 might represent as a novel and promising anti-pancreatic cancer strategy. PMID: 26084607
  27. results indicate that HDAC9 variant rs2107595 may be not associated with IS risk in southern Han Chinese PMID: 26093197
  28. Data show that miR-376a and HDAC9 expression are inversely correlated in hepatocellular carcinoma and suggest that HDAC9-mediated epigenetic modification may contribute to the down-regulation of the miR-376 cluster in hepatocellular carcinoma. PMID: 25613642
  29. Gene expression studies in peripheral blood mononuclear cells revealed increased mRNA levels of HDAC9. Analysis of human atherosclerotic plaques revealed no association between rs2107595 and specific plaque characteristics. PMID: 25388417
  30. The hydroxamic acid pan-HDAC inhibitor TSA synergistically inhibit the viability. PMID: 24562770
  31. The results elucidate the genetic etiology of lung adenocarcinoma by demonstrating that SNP rs10248565 in the HDAC9 gene may be a potential biomarker of cancer susceptibility. PMID: 24650256
  32. These results suggest that HDAC9 may be a suppressor and its downregulation might promote the progression process, especially in lung adenocarcinomas. PMID: 24427341
  33. study reports gene expression in skeletal muscle tissue of women with metabolic syndrome is enriched in inflammatory response-related genes; IL6R, HDAC9 and CD97 expression correlated negatively with insulin sensitivity; suggests a role for these 3 inflammatory genes in development of skeletal muscle insulin resistance in women PMID: 23771909
  34. These data suggest that HDAC9 variants may be selected for during cutaneous squamous cell carcinoma tumorigenesis PMID: 23784969
  35. In vivo sorafenib + HDAC inhibitor toxicity against tumors was increased. PMID: 23674352
  36. HDAC9 gene is significantly associated with large-vessel stroke risk in Chinese population. PMID: 23828597
  37. We propose that CtBP2 is an ovarian cancer oncogene that regulates gene expression program by modulating HDAC activity. PMID: 22945647
  38. SNP, rs12155400, in the histone deacetylase 9 gene (HDAC9) on chromosome 7, was associated with retinopathy in analysis of participants without hypertension PMID: 23393555
  39. Our results are consistent with the 7p21.1 association acting via promoting atherosclerosis, and consistent with alterations in HDAC9 expression mediating this increased risk. PMID: 23449258
  40. Regression models consistently identified rs2522129, rs2675231, and rs2389963 as having among the highest predictive values for explaining differences related to brain volume measures PMID: 22884548
  41. Dephosphorylation at a conserved SP motif governs cAMP sensitivity and nuclear localization of class IIa histone deacetylases HDAC4, 5 and 9 PMID: 23297420
  42. HDAC9 promotes angiogenesis and transcriptionally represses the endothelial cell miR-17-92 cluster. PMID: 23288173
  43. LBH589 and TSA may translationally regulate some HDAC encoding genes in pancreatic tumors. PMID: 22487525
  44. Data indicate a pronounced deregulation of HDAC genes HDAC9 and HDAC11 in patients with Philadelphia-negative chronic myeloproliferative neoplasms: essential thrombocythemia (ET), polycythemia vera (PV) and primary myelofibrosis (PMF). PMID: 21806350
  45. We identified a new association for large vessel stroke within HDAC9 on chromosome 7p21.1. PMID: 22306652
  46. Treated the seminoma-like cell line TCam-2 with the HDAC-inhibitor Depsipeptide. PMID: 21987446
  47. The results show that hdac9 is the third androgenic alopecia susceptibility gene PMID: 22032556
  48. HDAC9 acts as an epigenetic switch in effector T cell-mediated systemic autoimmunity. PMID: 21708950
  49. HDAC suppresses the activation of PPARgamma in the gastric carcinoma cell line SGC-7901. PMID: 19624894
  50. MITR plays a master switch role to balance osteogenic and adipogenic differentiation of MSCs through regulation of PPARgamma-2 transcriptional activity. PMID: 21247904

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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

To learn more about how to properly dissolve the lyophilized recombinant protein, please visit Lyophilization FAQs.

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