1. Signaling Pathways
  2. Apoptosis
  3. Caspase

Caspase (半胱天冬酶蛋白)

Caspase is a family of cysteine proteases that play essential roles in apoptosis (programmed cell death), necrosis, and inflammation. There are two types of apoptotic caspases: initiator (apical) caspases and effector (executioner) caspases. Initiator caspases (e.g., CASP2, CASP8, CASP9, and CASP10) cleave inactive pro-forms of effector caspases, thereby activating them. Effector caspases (e.g., CASP3, CASP6, CASP7) in turn cleave other protein substrates within the cell, to trigger the apoptotic process. The initiation of this cascade reaction is regulated by caspase inhibitors. CASP4 and CASP5, which are overexpressed in some cases of vitiligo and associated autoimmune diseases caused by NALP1 variants, are not currently classified as initiator or effector in MeSH, because they are inflammatory enzymes that, in concert with CASP1, are involved in T-cell maturation.

Caspase 亚型特异性产品:

  • Caspase 1

  • Caspase 2

  • Caspase 3

  • Caspase 4

  • Caspase 5

  • Caspase 6

  • Caspase 7

  • Caspase 8

  • Caspase 9

  • Caspase 10

  • Caspase 12

  • Caspase

  • Caspase 11

目录号 产品名 作用方式 纯度
  • HY-16658B
    Z-VAD-FMK Inhibitor ≥98.0%
    Z-VAD-FMK (Z-VAD(OH)-FMK) 是一种 pan caspase 抑制剂。Z-VAD-FMK 不抑制泛素 C 末端水解酶 L1 (UCHL1) 活性,即使浓度高达 440 μM。
  • HY-16658
    Z-VAD(OMe)-FMK Inhibitor ≥98.0%
    Z-VAD(OMe)-FMK (Z-Val-Ala-Asp(OMe)-FMK) 是一种不可逆的 pan-caspase 抑制剂。Z-VAD(OMe)-FMK 是泛素 C 末端水解酶 L1 (UCHL1) 抑制剂。Z-VAD(OMe)-FMK 通过靶向 UCHL1 活性位点对 UCHL1 进行不可逆地修饰。
  • HY-12466
    Z-DEVD-FMK Inhibitor ≥98.0%
    Z-DEVD-FMK 是一种特异性的不可逆的 caspase-3 抑制剂,IC50 为 18 μM。
  • HY-101297
    Z-IETD-FMK Inhibitor ≥98.0%
    Z-IETD-FMK (Z-IE(OMe)TD(OMe)-FMK) 是一种具有细胞渗透作用的选择性 caspase-8 抑制剂。Z-IETD-FMK 也是颗粒酶 B (granzyme B) 抑制剂。
  • HY-19696A
    Tauroursodeoxycholate Sodium Inhibitor 98.63%
    Tauroursodeoxycholate Sodium 是一种内质网应激抑制剂。Tauroursodeoxycholate 显著降低凋亡分子如 caspase-3caspase-12 表达。Tauroursodeoxycholate 也抑制 ERK
  • HY-103348
    Boc-Asp(OMe)-fluoromethyl ketone Inhibitor
    Boc-Asp(OME)-Fluoromethyl Keton 是一种广泛的 caspase 抑制剂,可抑制 Fas 介导的吞噬作用和氧化破裂抑制,但不影响 IL-8 的趋化活性。
  • HY-100676
    GRI977143 Inhibitor
    GRI977143 是特异性的 LPA2 受体的激动剂,其EC50 值为3.3 μM。
  • HY-129478
    TC11 Activator 98.04%
    TC11 是一种 MCL1 降解剂和 Caspase-9CDK1 激活剂。TC11 作为苯酞酰亚胺衍生物在结构上与免疫调节药物有关。在长时间有丝分裂阻滞期间,TC11 诱导 MCL1 降解导致凋亡性死亡。
  • HY-10396
    Emricasan Inhibitor 99.88%
    Emricasan (PF 03491390) 是一种口服有效的 不可逆 pan-caspase 抑制剂。Emricasan 抑制 Zika 病毒 (ZIKV) 诱导的 caspase-3 活性增加并保护了人类皮层神经祖细胞。
  • HY-P1001
    Ac-DEVD-CHO Inhibitor
    Ac-DEVD-CHO 是一种特异性 Caspase-3 抑制剂,Ki 值为 230 pM。
  • HY-19696
    Tauroursodeoxycholate Inhibitor ≥98.0%
    Tauroursodeoxycholate (TUDCA; UR 906; Taurolite) 是一种内质网应激抑制剂。Tauroursodeoxycholate 显著降低凋亡分子如 caspase-3caspase-12 表达。Tauroursodeoxycholate 也抑制 ERK
  • HY-107738
    Guggulsterone Activator 99.81%
    Guggulsterone 是一种植物甾醇,来自 Commiphora wightii 树的树胶脂。 Guggulsterone 通过下调抗细胞凋亡 (apoptosis) 基因产物 (IAP1,xIAP,Bfl-1/A1,Bcl-2,cFLIP,survivin),调节细胞周期蛋白 (cyclin D1,c-Myc),激活 caspases,JNK,抑制 Akt,抑制多种肿瘤细胞的生长并诱导细胞凋亡。Guggulsterone 通过调节几种转录因子介导基因表达,包括 NF-κB,STAT3,C /EBPα,雄激素受体 (androgen receptor) 和糖皮质激素受体(glucocorticoid receptors)。Guggulsterone,一种法尼醇 X 受体 (FXR) 拮抗剂,可降低 CDCA 诱导的 FXR 活化,Z- 和 E-Guggulsterone 的 IC50 分别为 17 和 15 μM。
  • HY-N0551
    Wedelolactone Inhibitor 99.91%
    Wedelolactone,是一种来自 Ecliptae herba 的天然产物,通过直接抑制 IKK 复合物来抑制 LPS 诱导的 caspase-11 表达。Wedelolactone 通过氧自由基清除机制抑制 5-脂氧合酶 (5-lipoxygenase, 5-Lox) (IC50~2.5 μM) 活性。Wedelolactone 通过下调 PKCε 诱导前列腺癌细胞中 caspase 依赖性细胞凋亡 (apoptosis) 而不抑制 Akt。具有抗癌,抗炎和抗氧化活性。
  • HY-P1009
    Z-YVAD-FMK Inhibitor ≥98.0%
    Z-YVAD-FMK 是一种具有细胞通透性 caspase-1caspase-4 抑制剂,具有抗炎和抗肿瘤活性。
  • HY-19696B
    Tauroursodeoxycholate dihydrate Inhibitor ≥98.0%
    Tauroursodeoxycholate dihydrate (TUDCA dihydrate; UR 906 dihydrate; Taurolite dihydrate) 是一种内质网应激抑制剂。Tauroursodeoxycholate 显著降低凋亡分子如 caspase-3caspase-12 表达。Tauroursodeoxycholate 也抑制 ERK
  • HY-N0605
    Ginsenoside Rh2 Activator ≥98.0%
    Ginsenoside Rh2 诱导 caspase-8caspase-9 活化。Ginsenoside Rh2 以多途径方式诱导癌细胞凋亡。
  • HY-B1193
    Terfenadine Activator 99.93%
    Terfenadine ((±)-Terfenadine) 是一种有效的 hERG 开放通道抑制剂, IC50为 204 nM。Terfenadine 也是一种 H1 组胺受体 (histamine receptor) 拮抗剂,通过调节 Ca2+ 稳态在黑素瘤细胞中起到有效的细胞凋亡诱导作用。 Terfenadine 诱导 ROS 依赖性细胞凋亡,同时激活 Caspase-4,-2,-9
  • HY-N0674A
    Dehydrocorydaline chloride Activator 98.64%
    Dehydrocorydaline chloride (13-Methylpalmatine chloride) 是一种生物碱。Dehydrocorydaline 调节 BaxBcl-2 蛋白表达;激活 caspase-7caspase-8,并使 PARP 失活。Dehydrocorydaline chloride 能增强 p38 MAPK 活化,具有抗炎、抗癌等功效。。Dehydrocorydaline chloride 具有强大的抗疟疾作用,并具低细胞毒性 (细胞生存力> 90%), P. falciparum 3D7 strain (IC50=38 nM)。
  • HY-N6979
    Crustecdysone Inhibitor 99.64%
    Crustecdysone (20-Hydroxyecdysone) 是一种天然存在的蜕皮激素,源于露水草 Cyanotis arachnoides C.B.Clarke, 可控制节肢动物的蜕皮和变态,它通过 20E 核受体复合物 EcR-USP 抑制半胱天冬酶 (Caspase) 活性并诱导自噬 (autophagy)。Crustecdysone 在心血管系统中具有调节或保护作用。Crustecdysone 是 Ecdysone (α-Ecdysone; HY-N0179) 的活性代谢物。
  • HY-111675
    Ac-FLTD-CMK Inhibitor 99.53%
    Ac-FLTD-CMK 是胃泌素 D (GSDMD) 衍生的抑制剂,是炎症性 caspases 的特异性抑制剂。Ac-FLTD-CMK 对 caspases-1 (IC50 为 46.7 nM),caspases-4 (IC50 为 1.49 μM),caspases-5 (IC50 为 329 nM) 和 caspases-11 均有效,但对凋亡相关的 caspase-3 无效。

Upon binding to their cognate ligand, death receptors such as Fas and TRAILR can activate initiator Caspases (Pro-caspase 8 and Pro-caspase 10) through dimerization mediated by adaptor proteins such as FADD and TRADD. Active Caspase 8 and Caspase 10 then cleave and activate the effector Caspase 3, 6 and 7, leading to apoptosis. ROS/DNA damage and ER stress trigger Caspase 2 activation. Active Caspase 2 cleaves and activates Caspase 3 and initiates apoptosis directly. Caspase 2, 8 and 10 can also cleave Bid, stimulate mitochondrial outer membrane permeabilization (MOMP) and initiate the intrinsic apoptotic pathway. Following MOMP, mitochondrial intermembrane space proteins such as Smac and Cytochrome C are released into the cytosol. Cytochrome C interacts with Apaf-1, triggering apoptosome assembly, which activates Caspase 9. Active Caspase 9, in turn, activates Caspase 3, 6 and 7, leading to apoptosis. Mitochondrial release of Smac facilitates apoptosis by blocking the inhibitor of apoptosis (IAP) proteins. 

 

Following the binding of TNF to TNFR1, TNFR1 binds to TRADD, which recruits RIPK1, TRAF2/5 and cIAP1/2 to form TNFR1 signaling complex I. Formation of the complex IIa and complex IIb is initiated either by RIPK1 deubiquitylation mediated by CYLD or by RIPK1 non-ubiquitylation due to depletion of cIAPs. The Pro-caspase 8 homodimer in complex IIa and complex IIb generates active Caspase 8. This active Caspase 8 in the cytosol then carries out cleavage reactions to activate downstream executioner caspases and thus induce classical apoptosis[1][2]

 

Reference:

[1]. Thomas C, et al. Caspases in retinal ganglion cell death and axon regeneration. Cell Death Discovery volume 3, Article number: 17032 (2017).
[2]. Brenner D, et al. Regulation of tumour necrosis factor signalling: live or let die. Nat Rev Immunol. 2015 Jun;15(6):362-74.

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