1. Cell Cycle/DNA Damage
    Epigenetics
  2. HDAC

HDAC

HDAC (Histone deacetylases) are a class of enzymes that remove acetyl groups (O=C-CH3) from an ε-N-acetyl lysine amino acid on ahistone, allowing the histones to wrap the DNA more tightly. This is important because DNA is wrapped around histones, and DNA expression is regulated by acetylation and de-acetylation. Its action is opposite to that of histone acetyltransferase. HDAC proteins are now also called lysine deacetylases (KDAC), to describe their function rather than their target, which also includes non-histone proteins. Together with the acetylpolyamine amidohydrolases and the acetoin utilization proteins, the histone deacetylases form an ancient protein superfamily known as the histone deacetylase superfamily.

View HDAC Pathway Map

HDAC Isoform Specific Products:

  • HDAC

  • HDAC1

  • HDAC2

  • HDAC3

  • HDAC4

  • HDAC5

  • HDAC6

  • HDAC7

  • HDAC8

  • HDAC9

  • HDAC10

  • HDAC11

  • HD1

  • HD2

HDAC 相关产品 (73):

Cat. No. Product Name Effect Purity
  • HY-15144
    Trichostatin A Inhibitor 99.53%
    Trichostatin A 是有效的,特异的组蛋白去乙酰化酶类型 I 和 II (HDAC class I/II) 抑制剂,对 HDAC 的 IC50 值为 1.8 nM。
  • HY-10221
    Vorinostat Inhibitor 99.90%
    Vorinostat 是一种有效的,可口服的 HDAC1HDAC2HDAC3 (Class I)HDAC7 (Class II)Class IV (HDAC11) 的抑制剂,对 HDAC1/3 的 ID50 值分别为 10 nM 和 20 nM。
  • HY-10224
    Panobinostat Inhibitor 98.42%
    Panobinostat 是一种可口服的组蛋白去乙酰化酶 (HDAC) 抑制剂,常用于抗癌症研究。
  • HY-12163
    Entinostat Inhibitor 99.65%
    Entinostat 是I型选择性的 HDAC 抑制剂,作用于 HDAC1HDAC2HDAC3IC50 分别为 243 nM,453 nM 和 248 nM。
  • HY-15149
    Romidepsin Inhibitor 99.52%
    Romidepsin 是一种有效的 HDAC1HDAC2 抑制剂,IC50 值分别为 36 nM 和 47 nM。
  • HY-111400
    SR-4370 Inhibitor 98.33%
    SR-4370 是一种有效的 HDAC 抑制剂,对 HDAC1,HDAC2,HDAC3,HDAC8 和 HDAC6 的 IC50 值分别为 0.13 μM,0.58 μM,0.006 μM,2.3 μM 和 3.4 μM。
  • HY-109015
    Tucidinostat Inhibitor 98.01%
    Tucidinostat 是一种有效的,可口服的 HDAC 第 I 类 HDAC1/2/3 和第 IIb 类 HDAC10 的抑制剂,IC50 值分别为 95,160,67 和 78 nM,对 HDAC8 和 HDAC11 的作用较弱 (IC50,733 nM,432 nM),对 HDAC4/5/6/7/9 无作用。
  • HY-104008
    ACY-957 Inhibitor
    ACY-957 是一种选择性的 HDAC1HDAC2 抑制剂,对 HDAC1/2/3 的 IC50 值分别为 7 nM,18 nM 和 1300 nM,对 HDAC4/5/6/7/8/9 无作用。
  • HY-12164
    Mocetinostat Inhibitor 99.49%
    Mocetinostat 是一种有效的,可口服的,亚型选择性的 HDAC (Class I/IV) 抑制剂,作用于 HDAC1HDAC2HDAC3HDAC11IC50 分别为 0.15,0.29,1.66 和 0.59 μM。 Mocetinostat 对 HDAC4,HDAC5,HDAC6,HDAC7 和 HDAC8 无作用.
  • HY-16026
    ACY-1215 Inhibitor 98.90%
    ACY-1215 是一种有效的选择 HDAC6 抑制剂,IC50 为 5 nM。ACY-1215 也抑制 HDAC1HDAC2HDAC3IC50 分别为 58,48 和 51 nM。
  • HY-10225
    Belinostat Inhibitor 99.97%
    Belinostat 是一种有效的 HDAC 抑制剂,作用于 HeLa 细胞提取物,IC50 为 27 nM。
  • HY-B0350A
    Sodium Butyrate Inhibitor >98.00%
    Sodium Butyrate 是组蛋白去乙酰化酶 (HDAC) 抑制剂,具有抗肿瘤作用。
  • HY-10585
    Valproic acid Inhibitor 98.67%
    Valproic acid 是一种 HDAC 抑制剂,IC50 值为 0.5-2 mM,抑制 HDAC1 的活性,(IC50,400 μM),同时可诱导 HDAC2 的降解;Valproic acid sodium salt 可用于癫痫、双相情感障碍和偏头痛等的研究。
  • HY-15433
    Quisinostat Inhibitor >98.0%
    Quisinostat (JNJ-26481585)是有口服活性的,高效的HDAC抑制剂,对HDAC1的IC50值为0.11 nM。
  • HY-13909
    RGFP966 Inhibitor 98.99%
    RGFP966 是一种选择性的 HDAC3 抑制剂,IC50 为 80 nM,浓度高达 15 μM时,对其他 HDAC 也没作用效果。
  • HY-10585A
    Valproic acid sodium salt Inhibitor >98.0%
    Valproic acid sodium salt 是一种 HDAC 抑制剂,IC50 值为 0.5-2 mM,抑制 HDAC1 的活性,(IC50,400 μM),同时可诱导 HDAC2 的降解;Valproic acid sodium salt 可用于癫痫、双相情感障碍和偏头痛等的研究。
  • HY-13428
    Tubacin Inhibitor 98.87%
    Tubacin 是一种有效的,选择性的 HDAC6 抑制剂,IC50 值为 4 nM,大约是对 HDAC1 的 350 倍。
  • HY-15224
    PCI-34051 Inhibitor 99.46%
    PCI-34051 是一种有效的选择性的 HDAC8 抑制剂,IC50 为 10 nM。
  • HY-50934
    CI-994 Inhibitor 99.08%
    CI-994 (Tacedinaline)是组蛋白脱乙酰酶(HDAC)的抑制剂,抑制重组HDAC 1, 2 and 3的IC50值分别为0.9, 0.9, 1.2 μM.
  • HY-18998
    LMK-235 Inhibitor 99.46%
    LMK-235 是一种有效的,选择性的 HDAC4/5 抑制剂,可抑制 HDAC5,HDAC4,HDAC6,HDAC1,HDAC2,HDAC11 和 HDAC8 的活性,IC50 值分别为 4.22 nM,11.9 nM,55.7 nM,320 nM,881 nM,852 nM 和 1278 nM,可用于癌症研究。
hdac-map.png

TCR, GPCR and HDAC II interaction: Diverse agonists act through G-protein-coupled receptors (GPCRs) to activate the PKC-PKD axis, CaMK, Rho, or MHC binding to antigens stimulates TCR to activate PKD, leading to phosphorylation of class II HDACs. Phospho-HDACs dissociate from MEF2, bind 14-3-3, and are exported to the cytoplasm through a CRM1-dependent mechanism. CRM1 is inhibited by leptomycin B (LMB). Release of MEF2 from class II HDACs allows p300 to dock on MEF2 and stimulate gene expression. Dephosphorylation of class II HDACs in the cytoplasm enables reentry into the nucleus[1].

 

TLR: TLR signaling is initiated by ligand binding to receptors. The recruitment of TLR domain-containing adaptor protein MyD88 is repressed by HDAC6, whereas NF-κB and MTA-1 can be negatively regulated by HDAC1/2/3 and HDAC2, respectively. Acetylation by HATs enhance MKP-1 which inhibits p38-mediated inflammatory responses, while HDAC1/2/3 inhibits MKP-1 activity. HDAC1 and HDAC8 repress, whereas HDAC6 promotes, IRF function in response to viral challenge. HDAC11 inhibits IL-10 expression and HDAC1 and HDAC2 represses IFNγ-dependent activation of the CIITA transcription factor, thus affecting antigen presentation[2][3].

 

IRNAR: IFN-α/β induce activation of the type I IFN receptor and then bring the receptor-associated JAKs into proximity. JAK adds phosphates to the receptor. STATs bind to the phosphates and then phosphorylated by JAKs to form a dimer, leading to nuclear translocation and gene expression. HDACs positively regulate STATs and PZLF to promote antiviral responses and IFN-induced gene expression[2][3].

 

Cell cycle: In G1 phase, HDAC, Retinoblastoma protein (RB), E2F and polypeptide (DP) form a repressor complex. HDAC acts on surrounding chromatin, causing it to adopt a closed chromatin conformation, and transcription is repressed. Prior to the G1-S transition, phosphorylation of RB by CDKs dissociates the repressor complex. Transcription factors (TFs) gain access to their binding sites and, together with the now unmasked E2F activation domain. E2F is then free to activate transcription by contacting basal factors or by contacting histone acetyltransferases, such as CBP, that can alter chromatin structure[4].

 

The function of non-histone proteins is also regulated by HATs/HDACs. p53: HDAC1 impairs the function of p53. p53 is acetylated under conditions of stress or HDAC inhibition by its cofactor CREB binding protein (CBP) and the transcription of genes involved in differentiation is activated. HSP90: HSP90 is a chaperone that complexes with other chaperones, such as p23, to maintain correct conformational folding of its client proteins. HDAC6 deacetylates HSP90. Inhibition of HDAC6 would result in hyperacetylated HSP90, which would be unable to interact with its co-chaperones and properly lead to misfolded client proteins being targeted for degradation via the ubiquitin-proteasome system[5][6].
 

Reference:

[1]. Vega RB, et al. Protein kinases C and D mediate agonist-dependent cardiac hypertrophy through nuclear export of histone deacetylase 5.Mol Cell Biol. 2004 Oct;24(19):8374-85.
[2]. Shakespear MR, et al. Histone deacetylases as regulators of inflammation and immunity. Trends Immunol. 2011 Jul;32(7):335-43.
[3]. Suliman BA, et al. HDACi: molecular mechanisms and therapeutic implications in the innate immune system.Immunol Cell Biol. 2012 Jan;90(1):23-32. 
[4]. Brehm A, et al. Retinoblastoma protein meets chromatin.Trends Biochem Sci. 1999 Apr;24(4):142-5.
https://www.ncbi.nlm.nih.gov/pubmed/10322419
[5]. Butler R, et al. Histone deacetylase inhibitors as therapeutics for polyglutamine disorders.Nat Rev Neurosci. 2006 Oct;7(10):784-96
[6]. Minucci S, et al. Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer.Nat Rev Cancer. 2006 Jan;6(1):38-51.

Isoform Specific Products

Your Search Returned No Results.

Sorry. There is currently no product that acts on isoform together.

Please try each isoform separately.