KLHL7 promotes TUT1 ubiquitination associated with nucleolar integrity: Implications for retinitis pigmentosa

Kim, Jae Hyun; Tsuruta, Fuminori; Okajima, Tomomi; Yano, Sarasa; Sato, Ban; Chiba, Tomoki

doi:10.1016/j.bbrc.2017.10.049

Cited by 17 publications

(10 citation statements)

References 36 publications

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“…KLHL7 forms a ubiquitin ligase complex and regulates ubiquitination [9,10]; however, there is a critical lack of knowledge of the targets of KLHL7 ubiquitination in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

“…The functions of many proteins are controlled by ubiquitination [3,4], and in cancer cells, abnormal ubiquitination may promote the activity of oncogenic pathways [5,6], enhance tumour proliferation, migration, invasion, angiogenesis, epithelial-mesenchymal transition and metastasis [7,8]. Kelch-like family member 7 (KLHL7), which is a member of the Kelch protein family associated with the development of retinitis pigmentosa [9,10], forms a ubiquitin ligase complex by binding to the BTB and BACK domains of Cullin3 (CUL3) [10,11]. This binding facilitates proteasome degradation of target proteins by enhancing E2 or E3 ligase activity and polyubiquitination [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Clinical and biological roles of Kelch-like family member 7 in breast cancer: a marker of poor prognosis

Kurozumi

Joseph

Sonbul

et al. 2018

Breast Cancer Res Treat

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“…KLHL7 forms a ubiquitin ligase complex and regulates ubiquitination [9,10]; however, there is a critical lack of knowledge of the targets of KLHL7 ubiquitination in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clinical and biological roles of Kelch-like family member 7 in breast cancer: a marker of poor prognosis

Kurozumi

Joseph

Sonbul

et al. 2018

Breast Cancer Res Treat

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“…In line with this, most high-throughput genome-scale RNAi or CRISPR-based screens identified TENT1 as an essential fitness gene [ 121 – 124 ]. TENT1 is dominantly localized in the nucleoplasm and nuclear speckle body-like structures and/or nucleolus [ 125 , 126 ]. Its localization in the nucleolus depends on an interaction with the NMP1 nucleolar protein and is reduced by ubiquitination by the Cullin-RING ubiquitin ligase complex subunit—KLHL7 protein [ 125 ].…”

Section: Tutases and Uridylationmentioning

confidence: 99%

“…TENT1 is dominantly localized in the nucleoplasm and nuclear speckle body-like structures and/or nucleolus [ 125 , 126 ]. Its localization in the nucleolus depends on an interaction with the NMP1 nucleolar protein and is reduced by ubiquitination by the Cullin-RING ubiquitin ligase complex subunit—KLHL7 protein [ 125 ]. TENT1 comprises several domains, whose organization is different from TUT4 and TUT7 ( figure 1 ) [ 127 , 128 ].…”

Section: Tutases and Uridylationmentioning

confidence: 99%

Terminal nucleotidyl transferases (TENTs) in mammalian RNA metabolism

Warkocki

Liudkovska

Gewartowska

et al. 2018

Phil. Trans. R. Soc. B

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In eukaryotes, almost all RNA species are processed at their 3′ ends and most mRNAs are polyadenylated in the nucleus by canonical poly(A) polymerases. In recent years, several terminal nucleotidyl transferases (TENTs) including non-canonical poly(A) polymerases (ncPAPs) and terminal uridyl transferases (TUTases) have been discovered. In contrast to canonical polymerases, TENTs' functions are more diverse; some, especially TUTases, induce RNA decay while others, such as cytoplasmic ncPAPs, activate translationally dormant deadenylated mRNAs. The mammalian genome encodes 11 different TENTs. This review summarizes the current knowledge about the functions and mechanisms of action of these enzymes.This article is part of the theme issue ‘5′ and 3′ modifications controlling RNA degradation’.

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“…They observed that the mutant KLHL7 protein decreased the translocation (from nucleolus) and ubiquitination of TUT1. 54 Thus, accumulation and mis localization of TUT1 due to mutations in KLHL7 create a disturbance to the RNA metabolism affecting the cells.…”

Section: Mechanisms Involved In Toxic Gain Of Function – Adrpmentioning

confidence: 99%

Autosomal dominant retinitis pigmentosa with toxic gain of function: Mechanisms and therapeutics

Narasimhan¹,

Murali²,

Krishnakumar³

et al. 2020

European Journal of Ophthalmology

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Autosomal dominant retinitis pigmentosa is a form of retinitis pigmentosa, an inherited retinal degenerative disorder characterized by progressive loss of photoreceptors eventually leading to irreversible loss of vision. Mutations in genes involved in the basic functions of the visual system give rise to this condition. These mutations can either lead to loss of function or toxic gain of function phenotypes. While autosomal dominant retinitis pigmentosa caused by loss of function can be ideally treated by gene supplementation with a single vector to address a different spectrum of mutations in a gene, the same strategy cannot be applied to toxic gain of function phenotypes. In toxic gain of function phenotypes, the mutation in the gene results in the acquisition of a new function that can interrupt the functioning of the wildtype protein by various mechanisms leading to cell toxicity, thus making a single approach impractical. This review focuses on the genes and mechanisms that cause toxic gain of function phenotypes associated with autosomal dominant retinitis pigmentosa and provide a bird’s eye view on current therapeutic strategies and ongoing clinical trials.

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KLHL7 promotes TUT1 ubiquitination associated with nucleolar integrity: Implications for retinitis pigmentosa

Cited by 17 publications

References 36 publications

Clinical and biological roles of Kelch-like family member 7 in breast cancer: a marker of poor prognosis

Clinical and biological roles of Kelch-like family member 7 in breast cancer: a marker of poor prognosis

Terminal nucleotidyl transferases (TENTs) in mammalian RNA metabolism

Autosomal dominant retinitis pigmentosa with toxic gain of function: Mechanisms and therapeutics

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