1. Apoptosis
  2. Caspase

Caspase

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.

View Caspase Pathway Map

Caspase Isoform Specific Products:

  • Caspase 1

  • Caspase 2

  • Caspase 3

  • Caspase 4

  • Caspase 5

  • Caspase 6

  • Caspase 7

  • Caspase 8

  • Caspase 9

  • Caspase 10

  • Caspase 12

  • Caspase

Caspase 相关产品 (19):

Cat. No. Product Name Effect Purity
  • HY-16658
    Z-VAD(OMe)-FMK Inhibitor >98.0%
    Z-VAD(OMe)-FMK 是一种可渗透细胞的不可逆 pan-caspase 抑制剂。
  • HY-13205
    VX-765 Inhibitor 99.99%
    VX-765 是一种口服活性的 IL-转化酶/caspase-1 抑制剂,抑制 IL-1β 释放。
  • 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-12305
    Q-VD-OPh Inhibitor 99.26%
    Q-VD-OPha 是一种不可逆的泛胱天蛋白酶 (caspase) 抑制剂,具有高效的抗凋亡能力。抑制胱天蛋白酶 7 的 IC50 值别为 48 nM,抑制胱天蛋白酶 1,3,8,9,10,12 的 IC50 值在 25-400 nM 之间。Q-VD-OPha 能透过血脑屏障。
  • HY-10396
    Emricasan Inhibitor 99.73%
    Emricasan 是一种不可逆的 pan-caspase 抑制剂。
  • HY-12412
    ML132 Inhibitor
    ML132 (NCGC 00185682)是有效和选择性的 caspase 1 抑制剂,IC50 值为 0.316 nM。
  • HY-N1157
    Thevetiaflavone Inhibitor
    Thevetiaflavone 可以上调 Bcl‑2 的表达,下调 Baxcaspase-3 的表达。
  • HY-19696
    Tauroursodeoxycholate Inhibitor
    Tauroursodeoxycholate 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-101297
    Z-IETD-FMK Inhibitor >98.0%
    Z-IETD-FMK是选择性和细胞可渗透的胱天蛋白酶 (caspase 8) 抑制剂。
  • HY-19696A
    Tauroursodeoxycholate Sodium Inhibitor >98.0%
    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-P1001
    Ac-DEVD-CHO Inhibitor 98.84%
    Ac-DEVD-CHO 是一种特异性 Caspase-3 抑制剂,Ki 值为 230 pM.
  • HY-13523
    PAC-1 Activator
    PAC-1 是一种 procaspase-3 激活剂,诱导癌细胞凋亡,EC50 为 2.08 μM。
  • HY-13229
    BOC-D-FMK Inhibitor
    Boc-D-FMK是可渗透细胞,不可逆的,泛半胱天冬酶抑制剂。抑制TNF-α诱导的细胞凋亡的IC50值为39 µM。
  • HY-N2027
    Taurochenodeoxycholic acid Activator 99.80%
    Taurochenodeoxycholic acid是动物胆汁酸的主要生物活性物质之一。
  • HY-N0605
    Ginsenoside Rh2 Activator >98.0%
    Ginsenoside Rh2 是从 Ginseng 根中分离出来的。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-103667
    2-HBA Activator 98.83%
    2-HBA 是一个有效的 NAD(P)H: 醌受体氧化还原酶 1 (NQO1) 诱导剂,也可以激活半胱天冬酶-3 (caspase-3) 和半胱天冬酶-10 (caspase-10)。
  • HY-10397
    EP1013 Inhibitor
    EP1013 是一种广谱的 caspase 选择性抑制剂,可用于 1 型糖尿病研究。
  • HY-100894
    Biotin-VAD-FMK Inhibitor >98.0%
    Biotin-VAD-FMK是可渗透细胞的,不可逆的,由生物素标记的胱天蛋白酶抑制剂,用于鉴定细胞裂解物中的半胱天冬酶活性。
  • HY-N0905
    Ginsenoside Rh4 Activator 98.40%
    Ginsenoside Rh4 是从 Panax notoginseng 中获得的稀有皂苷。Ginsenoside Rh4 激活 Baxcaspase 3caspase 8caspase 9。Ginsenoside Rh4 还诱导自噬。
caspase-map.png

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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