USP45

Last update 08 May 2025

Basic Info

Synonyms

Deubiquitinating enzyme 45, MGC14793, Ubiquitin carboxyl-terminal hydrolase 45

+ [4]

Introduction

Catalyzes the deubiquitination of SPDL1 (PubMed:30258100). Plays a role in the repair of UV-induced DNA damage via deubiquitination of ERCC1, promoting its recruitment to DNA damage sites (PubMed:25538220). May be involved in the maintenance of photoreceptor function (PubMed:30573563). May play a role in normal retinal development (By similarity). Plays a role in cell migration (PubMed:30258100).

100 Clinical Results associated with USP45

100 Translational Medicine associated with USP45

0 Patents (Medical) associated with USP45

111

Literatures (Medical) associated with USP45

05 May 2025·Journal of Cell Biology

Correction: The deubiquitinase USP45 inhibits autophagy through actin regulation by Coronin 1B

Author: Chen, Guang-Chao ; Lin, Yuchieh Jay ; Huang, Li-Ting ; Ke, Po-Yuan

05 May 2025·Journal of Cell Biology

The deubiquitinase USP45 inhibits autophagy through actin regulation by Coronin 1B

Article

Author: Lin, Yuchieh Jay ; Ke, Po-Yuan ; Chen, Guang-Chao ; Huang, Li-Ting

The autophagy–lysosomal system comprises a highly dynamic and interconnected vesicular network that plays a central role in maintaining proteostasis and cellular homeostasis. In this study, we uncovered the deubiquitinating enzyme (DUB), dUsp45/USP45, as a key player in regulating autophagy and lysosomal activity in Drosophila and mammalian cells. Loss of dUsp45/USP45 results in autophagy activation and increased levels of V-ATPase to lysosomes, thus enhancing lysosomal acidification and function. Furthermore, we identified the actin-binding protein Coronin 1B (Coro1B) as a substrate of USP45. USP45 interacts with and deubiquitinates Coro1B, thereby stabilizing Coro1B levels. Notably, the ablation of USP45 or Coro1B promotes the formation of F-actin patches and the translocation of V-ATPase to lysosomes in an N-WASP-dependent manner. Additionally, we observed positive effects of dUsp45 depletion on extending lifespan and ameliorating polyglutamine (polyQ)-induced toxicity in Drosophila. Our findings highlight the important role of dUsp45/USP45 in regulating lysosomal function by modulating actin structures through Coro1B.

01 Jan 2025·Clinical Lymphoma Myeloma and Leukemia

Familial Multiple Myeloma: Insights From Epidemiology and Underlying Germline Genetic Predisposition to the Clinic

Review

Author: Akkus, Erman ; Tuncalı, Timur ; Beksac, Meral

Familial multiple myeloma (MM) is a relatively rare entity. Data on epidemiology, underlying germline genetic predisposition, and clinical features of familial MM continue to expand, especially in recent years. The risk of MM has been reported to be increased by 2 to 4 times among first-degree relatives of MM patients along with monoclonal gammopathy of undetermined significance (MGUS), other hematological malignancies, and several solid tumors by multiple groups. The association between MM risk and having a first-degree relative with a history of MM is stronger among African Americans/Blacks (OR = 5.52, 95% CI: 1.87-16.28) than European Americans/Whites (OR = 1.26, 95% CI: 0.75-2.10). Although data on clinical features and prognosis of familial cases are limited, preliminary data suggest a better prognosis among familial cases. Sequencing studies in familial cases have discovered rare disease-causing variants among which CDKN2A, USP45, MYH14, EPOR, HERC1, KLHL18, and KLHDC3 are shared by independent groups. Some of these candidate genes possess functions related to myelomagenesis such as B-cell development, immunoglobulin gene regulation, immune pathways, DNA damage/repair, ubiquitination, and cell adhesion mechanisms. Our group has recently completed an analysis among our Turkish MM families to confirm the findings of the International Consortium. The odds ratio (OR) for single nucleotide polymorphism rs28199 in nonfamilial MM cases compared to healthy control was 1.18, with an OR of 2.86 in familial MM cases compared to nonfamilial cases. Despite the accumulation of data, most questions remain to be answered. Future studies may elucidate underlying biological mechanisms, and develop polygenic risk scores, leading advancements in prognostic evaluation and clinical management.

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USP45

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