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Literature summary for 3.4.19.12 extracted from

  • Ichikawa, T.; Li, J.; Dong, X.; Potts, J.D.; Tang, D.Q.; Li, D.S.; Cui, T.
    Ubiquitin carboxyl terminal hydrolase L1 negatively regulates TNFalpha-mediated vascular smooth muscle cell proliferation via suppressing ERK activation (2010), Biochem. Biophys. Res. Commun., 391, 852-856.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Rattus norvegicus Q00981 adult Sprague-Dawley rats
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Source Tissue

Source Tissue Comment Organism Textmining
aorta vascular smooth muscle cells. UCH-L1 is up-regulated in injured arteries Rattus norvegicus
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vascular smooth muscle cell
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Rattus norvegicus
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Synonyms

Synonyms Comment Organism
ubiquitin carboxyl terminal hydrolase L1
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Rattus norvegicus
UCH-L1
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Rattus norvegicus

Expression

Organism Comment Expression
Rattus norvegicus TNFalpha up-regulates UCH-L1via a translational regulation to inhibit ERK activity, thereby providing a negative feedback to control its growth promoting signaling in vascular smooth muscle cells up

General Information

General Information Comment Organism
malfunction UCH-L1 is up-regulated in injured arteries, via posttranscriptional regulation, and local gene delivery of UCH-L1 inhibited vascular lesion formation with suppression of inflammatory responses in vasculature. ERK activation also contributes to the growth inhibitory effect of UCH-L1 in TNFalpha-inflamed vascular smooth muscle cells Rattus norvegicus
physiological function UCH-L1 appears to be a multi-functional protein and exerts cell type and/or tissue specific actions Rattus norvegicus