Literature summary for 3.4.19.12 extracted from

Read, N.C.; Gutsol, A.; Holterman, C.E.; Carter, A.; Coulombe, J.; Gray, D.A.; Kennedy, C.R.
Ubiquitin C-terminal hydrolase L1 deletion ameliorates glomerular injury in mice with ACTN4-associated focal segmental glomerulosclerosis (2014), Biochim. Biophys. Acta, 1842, 1028-1040.

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
podocyte	UCHL1 is expressed in podocytes of K256E-ACTN4pod+/UCHL1+/+ mice	Mus musculus	-

Synonyms

Synonyms	Comment	Organism
ubiquitin C-terminal hydrolase L1	-	Mus musculus
UCHL1	-	Mus musculus

General Information

General Information	Comment	Organism
malfunction	10-week-old K256E-ACTN4pod+/UCHL1-/- mice exhibit reduced albuminuria, glomerulosclerosis, foot process effacement, glomerular basement membrane thickening, glomerular and tubular cell apoptosis, and ameliorated renal pathology. Observations coincide with decreased polyubiquitinated protein levels and increased K256E-alpha-actinin-4 levels in K256E-ACTN4pod+/UCHL1-/-mice kidneys, suggesting impaired proteolysis of K256E-alpha-actinin-4	Mus musculus

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Release 2023.1 (January 2023)