Caspase 12

Caspase-12 belongs to the inflammatory caspase group, but its biology differs from caspase-1, -4, -5, and -11 because it can attenuate endotoxin-induced cytokine production rather than directly promote cytokine maturation^[1]^[2]. Mechanistically, human full-length Caspase-12 reduced lipopolysaccharide-stimulated cytokine production in ex vivo whole blood and was linked to severe sepsis risk in African American individuals^[1]. In viral immunity, mouse Caspase-12 controlled West Nile virus infection by regulating TRIM25-mediated RIG-I ubiquitination and type I interferon production^[3]. ER-stress studies connect Caspase-12 with apoptosis, because overexpressed full-length caspase-12 underwent processing and ER-stress models showed caspase-12-associated caspase-3 activation^[4]^[5]. In intestinal inflammation, IKKα loss increased unfolded protein response and caspase-12 activation, reducing protective IL-18 secretion during acute colitis^[6]. Compared with caspase-1 and caspase-11, however, triple-knockout mouse data found no additional caspase-12 contribution to LPS response, apoptosis, necroptosis, or tunicamycin-induced ER stress in that model^[7]. For experimental applications, caspase-12 inhibition with Z-ATAD-FMK reduced oxygen-glucose-deprivation injury, apoptosis, NLRP3, caspase-1, IL-1β, and cleaved caspase-3 in primary astrocytes^[8].

References:

[1]. Saleh M, et al. Differential modulation of endotoxin responsiveness by human caspase-12 polymorphisms. Nature. 2004 May 6;429(6987):75-9. [Content Brief]

[2]. Martinon F, et al. Inflammatory caspases and inflammasomes: master switches of inflammation. Cell Death Differ. 2007 Jan;14(1):10-22. [Content Brief]

[3]. Wang P, et al. Caspase-12 controls West Nile virus infection via the viral RNA receptor RIG-I. Nat Immunol. 2010 Oct;11(10):912-9. [Content Brief]

[4]. Kalai M, et al. Regulation of the expression and processing of caspase-12. J Cell Biol. 2003 Aug 4;162(3):457-67. [Content Brief]

[5]. Hitomi J, et al. Apoptosis induced by endoplasmic reticulum stress depends on activation of caspase-3 via caspase-12. Neurosci Lett. 2004 Mar 4;357(2):127-30. [Content Brief]

[6]. Diamanti MA, et al. IKKα controls ATG16L1 degradation to prevent ER stress during inflammation. J Exp Med. 2017 Feb;214(2):423-437. [Content Brief]

[7]. Salvamoser R, et al. Characterisation of mice lacking the inflammatory caspases-1/11/12 reveals no contribution of caspase-12 to cell death and sepsis. Cell Death Differ. 2019 Jun;26(6):1124-1137. [Content Brief]

[8]. Liu L, et al. Inhibiting Caspase-12 Mediated Inflammasome Activation protects against Oxygen-Glucose Deprivation Injury in Primary Astrocytes. Int J Med Sci. 2020 Jul 19;17(13):1936-1945. [Content Brief]

Caspase 12 Inhibitors (3)

Caspase 12 Related Products (3):

By Type:	Pan (3)

Cat. No.	Product Name	Effect	Purity

HY-12305

Q-VD-OPh	Inhibitor	99.92%
Q-VD-OPh is an irreversible pan-caspase inhibitor with potent antiapoptotic properties; inhibits caspase 7 with an IC₅₀ of 48 nM and 25-400 nM for other caspases including caspase 1, 3, 8, 9, 10, and 12. Q-VD-OPh can inhibits HIV infection. Q-VD-OPh is able to cross the blood-brain barrier.

HY-19696

Tauroursodeoxycholate	Inhibitor	99.93%
Tauroursodeoxycholate (Tauroursodeoxycholic acid) is an orally active endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.

HY-19696A

Tauroursodeoxycholate sodium	Inhibitor	98.40%
Tauroursodeoxycholate (Tauroursodeoxycholic acid; TUDCA) sodium is an endoplasmic reticulum (ER) stress inhibitor. Tauroursodeoxycholate significantly reduces expression of apoptosis molecules, such as caspase-3 and caspase-12. Tauroursodeoxycholate also inhibits ERK.

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