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    1. Cell Cycle/DNA Damage
    2. 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 (84):

    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是一种非选择性组蛋白去乙酰化酶 (HDAC) 抑制剂。
    • HY-12163
      Entinostat Inhibitor 99.65%
      Entinostat 选择性,可口服的 HDAC class I 抑制剂,抑制 HDAC1HDAC2HDAC3IC50 分别为 243 nM,453 nM 和 248 nM。
    • HY-15149
      Romidepsin Inhibitor 99.98%
      Romidepsin 是一种有效的 HDAC1HDAC2 抑制剂,IC50 值分别为 36 nM 和 47 nM。
    • HY-114483
      AES-135 Inhibitor
      AES-135 是一种有效的 HDAC 抑制剂,对 HDAC3HDAC6HDAC11IC50 值分别为 654,190 和 636 nM。具有抗肿瘤作用。
    • HY-112908
      RTS-V5 Inhibitor
      RTS-V5是HDAC/蛋白酶体的抑制剂,对HDAC1,HDAC2,HDAC3,HDAC6,HDAC8的IC50分别为6.9,18,15,0.27,0.53 μM。
    • HY-114414
      HDACs/mTOR Inhibitor 1 Inhibitor
      HDACs/mTOR Inhibitor 1 是组蛋白去乙酰酶抑制剂 (HDAC) 和哺乳动物雷帕霉素 (mTOR) 的双重抑制剂,有望用于治疗恶性血液病,其对 HDAC1、HDAC6、mTOR 和 PI3Kα 的IC50 值分别为 0.19 nM、1.8 nM、1.2 nM 和 >500 nM。HDACs/mTOR Inhibitor 1 能够引起G0/G1 期的细胞阻滞,诱导肿瘤细胞凋亡,在体内毒性较低。
    • 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-16026
      Ricolinostat Inhibitor 99.35%
      Ricolinostat (ACY-1215) 是一种有效,选择性的 HDAC6 抑制剂,IC50 为 5 nM。ACY-1215 也可抑制 HDAC1HDAC2HDAC3IC50 分别为 58,48 和 51 nM。
    • HY-B0350A
      Sodium Butyrate Inhibitor >98.00%
      Sodium Butyrate是一种短链脂肪酸,可以抑制组蛋白去乙酰化酶
    • HY-12164
      Mocetinostat Inhibitor 99.81%
      Mocetinostat (MGCD0103)是一种有效,可口服和同种型选择性的 HDAC (Class I/IV) 抑制剂,抑制HDAC1HDAC2HDAC3HDAC11IC50分别为0.15,0.29,1.66 和 0.59 μM。 Mocetinostat对HDAC4,HDAC5,HDAC6,HDAC7或HDAC8没有抑制作用。
    • HY-13755
      Sulforaphane Inhibitor 98.90%
    • HY-13909
      RGFP966 Inhibitor 98.99%
      RGFP966 是高选择性的 HDAC3 抑制剂,IC50 为 80 nM。在15 μM时对其他HDAC无抑制作用。
    • 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-15433
      Quisinostat Inhibitor >98.0%
      Quisinostat (JNJ-26481585)是有口服活性,高效的 HDAC 抑制剂,对HDAC1的 IC50 值为0.11 nM。
    • HY-10225
      Belinostat Inhibitor 99.97%
      Belinostat 是一种有效的 HDAC 抑制剂,在 HeLa 细胞提取物中的 IC50 为 27 nM。
    • HY-10585A
      Valproic acid sodium salt Inhibitor >98.0%
      Valproic acid sodium salt是一种用于治疗癫痫,双相情感障碍和偏头痛的抗惊厥药。 Valproic acid抑制组蛋白脱乙酰基酶1 (HDAC1)IC50 为 0.4 mM。
    • HY-13522
      Fimepinostat Inhibitor 99.95%
      Fimepinostat (CUDC-907) 有效抑制 I 型 PI3K 及 I 和 II 型 HDAC 酶,作用于 PI3Kα/PI3Kβ/PI3Kδ 和 HDAC1/HDAC2/HDAC3/HDAC10 ,IC50 分别为 19/54/39 nM 和 1.7/5.0/1.8/2.8 nM。
    • HY-15654
      Sodium phenylbutyrate Inhibitor 99.75%
      Sodium phenylbutyrate 是一种组蛋白去乙酰化酶 (HDAC) 和内质网应激 (ER) 抑制剂,可用于癌症和感染等疾病的研究。

    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].


    [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.
    [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

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    Please try each isoform separately.