3.4.22.43	malfunction	RNAi-mediated depletion of the enzyme effectively abrogates ectopic E2F1-induced apoptosis, coupled with reduced lysosomal membrane permeabilization and mitochondrial membrane depolarization. Enzyme knockdown also inhibits apoptosis mediated by the endogenous E2F1 activated by DNA damage. Enzyme depletion in cancer cells results in inhibition of histone deacetylase inhibitor-induced apoptosis	
3.4.22.43	malfunction	increased cathepsin V promoted the degradation of DUSP6 and DUSP7, phosphorylation and subsequent nuclear translocation of ERK1/2, phosphorylation of STAT1 and expression of interleukin (IL)-6, IL-8 and TNF-alpha	
3.4.22.43	malfunction	lack of cathepsins prevent the development of lung granulomas in a mouse model of Besnier-Boeck-Schaumann (BBS) disease, sarcoidosis. Cathepsin V (Cath V) in bronchoalveolar lavage fluid (BALF) in humans	
3.4.22.43	malfunction	melanosome degradation is suppressed in CTSV knockdown cells. Inhibition of CTSV expression increases melanosome accumulation in HaCaT keratinocytes. The rate of melanosome degradation is reduced in CTSV knockdown keratinocytes	
3.4.22.43	metabolism	cathepsin V participates in the production of enkephalin and neuropeptide Y neurotransmitters in secretory vesicles	
3.4.22.43	metabolism	cathepsin V and endostatin may represent an index of pulmonary sarcoidosis activity	
3.4.22.43	metabolism	effects of cathepsin V on the dual-specificity protein phosphatases (DUSPs) and MAPK pathways	
3.4.22.43	physiological function	CTSV is involved in the breakdown of corneodesmosomal proteins	
3.4.22.43	physiological function	expression of CTSV rescues the reduced frequency of CD4+ T cells in cysteine protease cathepsin L-deficient mice with H-2b haplotype	
3.4.22.43	physiological function	cathepsin like 2 is required for E2F1-induced apoptosis by engaging lysosomal membrane permeabilization. Its level also modulates the cellular sensitivity to histone deacetylase inhibitor	
3.4.22.43	physiological function	enzyme cathepsin V (CTSV) is involved in melanosome degradation in the keratinocytes derived from lightcolored skin. It is one of the factors regulating pigmentation	
3.4.22.43	physiological function	exogenous cathepsin V protein protects human cardiomyocytes from angiotensin II-induced hypertrophy, human cardiomyocytes hypertrophic cardiomyopathy (HCM) as a cell model to investigate the effects of exogenous CTSV on Ang II-induced cardiac cell hypertrophy, overview. Analysis of the mechanism of CTSV cardioprotection, overview. Exogenous CTSV inhibits Ang II-induced hypertrophy in HCM cells by inhibiting PI3K/Akt/mTOR	
3.4.22.43	physiological function	HIV protease inhibitor saquinavir targets the interaction of cathepsin V with TLR4/MyD88	
3.4.22.43	physiological function	L-homocysteine-induced cathepsin V mediates the vascular endothelial inflammation in hyperhomocysteinaemia. Cathepsin V, specifically expressed in humans, is involved in vascular diseases through its elastolytic and collagenolytic activities. Cathepsin V mediates the L-homocysteine-induced upregulation of inflammatory cytokines