Literature summary for 3.4.22.64 extracted from

Miao, N.; Yin, F.; Xie, H.; Wang, Y.; Xu, Y.; Shen, Y.; Xu, D.; Yin, J.; Wang, B.; Zhou, Z.; Cheng, Q.; Chen, P.; Xue, H.; Zhou, L.; Liu, J.; Wang, X.; Zhang, W.; Lu, L.
The cleavage of gasdermin D by caspase-11 promotes tubular epithelial cell pyroptosis and urinary IL-18 excretion in acute kidney injury (2019), Kidney Int., 96, 1105-1120.

Search for more literature for 3.4.22.64

Application

Application	Comment	Organism
medicine	gasdermin D (GSDMD)-dependent pyroptosis mediated by caspase-11 might be a target in preventing the loss of renal tubular epithelial cells and inflammation in acute kidney injury (AKI)	Mus musculus

Protein Variants

Protein Variants	Comment	Organism
additional information	generation of Casp-11-/- mice. Cisplatin-induced tubular dilation, loss of brush border, cast formation, and cell lysis in tubules are significantly ameliorated in Casp-11-/- mice. The level of urinary IL-18 is significantly suppressed in Casp-11-/- mice compared with wild-type mice after cisplatin treatment. Deletion of caspase-11 suppresses the infiltration of macrophages and neutrophils in cisplatin-induced acute kidney injury	Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
gasdermin D + H2O	Mus musculus	-	N-terminal domain of gasdermin D + C-terminal domain of gasdermin D	-	?

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	P70343	cf. caspase-4, EC 3.4.22.57	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
kidney	-	Mus musculus	-
macrophage	-	Mus musculus	-
neutrophil	-	Mus musculus	-
renal tubular epithelial cell	-	Mus musculus	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
gasdermin D + H2O	-	Mus musculus	N-terminal domain of gasdermin D + C-terminal domain of gasdermin D	-	?

Expression

Organism	Comment	Expression
Mus musculus	caspase-11 is upregulated of by either cisplatin or ischemia-reperfusion	up

General Information

General Information	Comment	Organism
malfunction	caspase-11 knockout mice exhibit attenuated deterioration of renal functional, reduced tubular damage, reduced macrophage and neutrophil infiltration, and decreased urinary IL-18 excretion after cisplatin treatment. Expression of caspase-11 is significantly increased after cisplatin or hypoxia-reoxygenation treatment. Knockout of GSDMD suppresses the excretion of IL-18 in urine after cisplatin treatment	Mus musculus
metabolism	caspase-11/GSDMD dependent tubule cell pyroptosis plays a significant role in initiating tubular cell damage, urinary IL-18 excretion and renal functional deterioration in acute kidney injury	Mus musculus
physiological function	caspase-11 is a cysteine protease that promotes cell pyroptosis. Cleavage of gasdermin D by caspase-11 promotes tubular epithelial cell pyroptosis and urinary IL-18 excretion in acute kidney injury. Inflammation and tubular cell death are the hallmarks of acute kidney injury. Upregulation of caspase-11 by either cisplatin or ischemia-reperfusion leads to cleavage of gasdermin D (GSDMD) into GSDMD-N, which translocates to the plasma membrane, thus triggering cell pyroptosis, and facilitates IL-18 release in primary cultured renal tubular cells. GSDMD is the specific substrate of caspasae-11 and the molecular biomarker of pyroptosis	Mus musculus

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Release 2026.1 (March 2026)