3.4.22.57: caspase-4
This is an abbreviated version!
For detailed information about caspase-4, go to the full flat file.
Word Map on EC 3.4.22.57
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3.4.22.57
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inflammasome
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pyroptosis
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chop
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lps
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caspase-5
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non-canonical
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stress-mediated
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gsdmd
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glucose-regulated
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perk
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stress-associated
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pyrin
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gadd153
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aif
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salubrinal
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speck-like
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atf-6
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eif2alpha
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pkr-like
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gasdermin-d
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inflammasome-mediated
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medicine
- 3.4.22.57
- inflammasome
-
pyroptosis
-
chop
- lps
- caspase-5
-
non-canonical
-
stress-mediated
-
gsdmd
-
glucose-regulated
-
perk
-
stress-associated
- pyrin
-
gadd153
- aif
- salubrinal
-
speck-like
- atf-6
- eif2alpha
-
pkr-like
-
gasdermin-d
-
inflammasome-mediated
- medicine
Reaction
strict requirement for Asp at the P1 position. It has a preferred cleavage sequence of Tyr-Val-Ala-Asp-/- but also cleaves at Asp-Glu-Val-Asp-/- =
Synonyms
C14.007, Cas4, CASP-4, CASP4, caspase 4, caspase-4, ICE(rel)-II, ICH-2 protease, ICH-3 protease, ICH3 protease, TX, TX protease
ECTree
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General Information
General Information on EC 3.4.22.57 - caspase-4
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evolution
malfunction
physiological function
additional information
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elevated caspase activity in Pt1 cells is an outcome of increased caspase-4 activation
evolution
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caspase-4 is a member of the caspase family and a member of the interleukin-1beta coverting enzyme subfamily
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overexpression of wild-type caspase-4 results in cytotoxicity, reflected by slightly enhanced amounts of beta-actin in the supernatant
malfunction
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when caspase-4 activity is blocked by the dominant negative form of nuclear factor-kappaB, Fas-induced cell death is substantially reduced
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caspase-4 directly activates caspase-9 in endoplasmic reticulum stress-induced apoptosis in SH-SY5Y cells, interaction between caspase-4 and caspase-9 in endoplasmic reticulum stress-induced apoptosis, overview
physiological function
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caspase-4 is a member of the inflammatory family of caspases involved in the regulation of the endoplasmic reticulum stress response, autophagy and cell survival. Cell death is occurring through a caspase-independent mechanism
physiological function
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caspase-4 is involved in endoplasmic reticulum stress-induced apoptosis and is required for activation of inflammasomes. Caspase-4 expression is required for UVB-induced activation of proIL-1beta and for unconventional protein secretion by skin-derived keratinocytes, requiring expression of the nucleotide-binding domain leucine-rich repeat containing, Pyrin domain containing-3 inflammasome. Caspase-4 supports activation of caspase-1 and proIL-1beta processing in COS-1 cells
physiological function
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acute inflammatory cell death in the intestinal tract is mediated by caspase-4
physiological function
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acute inflammatory cell death in the intestinal tract is mediated by caspase-4
physiological function
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caspase-4 activity is required for Fas-induced cell apoptosis
physiological function
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caspase-4 is involved in endotoxin sensitivity. Caspase-4 can support activation of caspase-1 and secretion of interleukin-1beta and interleukin-18 in response to priming signals (LPS or Pam3CSK4) alone, without the need for second signals to stimulate the assembly of the inflammasome
physiological function
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caspase-4 is required for maturation of pro-interleukin-1beta through activation of caspase-1 in keratinocytes
physiological function
caspase-4 and caspase-5 are the key determinants of one-step inflammasome activation in human monocyte. The contribute to TLR4-mediated IL-1alpha/beta release from human monocytes
physiological function
caspase-4 drives inflammasome responses to Francisella novicida infection in human macrophages. Caspase-4 triggers Francisella novicida-mediated, gasdermin D dependent pyroptosis and activates the NLRP3 inflammasome
physiological function
caspase-4 is a receptor for intracellular LPS, and induces non-canonical inflammasome formation and pyroptosis. Caspase-4 disaggregates lipopolysaccharide micelles via LPS-CARD interaction
physiological function
caspase-4 mediates non-canonical activation of the NLRP3 inflammasome in human myeloid cells
physiological function
human caspase-4 as a critical regulator of noncanonical inflammasome activation that initiates defense against gram-negative bacterial pathogens in primary human macrophages. Caspase-4 mediates IL-1alpha release and cell death