Редактирование: RNF8 (раздел)

==Publications==

{{medline-entry
|title=Expression of [[RNF8]] on cochlear apoptosis and aging in mice of different ages.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30915826
|abstract=This study aimed to investigate the role of [[RNF8]] (RING finger protein 8) in DNA damage repair in mice of different ages, and to provide new insight into the pathology and treatment of senile deafness. Sixteen C57BL/6J mice aged 8 weeks, 16 weeks and 32 weeks were obtained by paired reproduction. The mice of three age groups were equally divided into two groups, named experimental group ([[RNF8]] gene knockout) and control group (no knockout). The cochlear hair cells, stria vascularis and spiral ganglion cells were observed by HE (hematoxylin-eosin) staining. The degree of DNA damage and the related expressions were observed by immunofluorescence γ-[[H2AX]] staining and 8-OH immunohistochemical staining, and the aging of damaged cells was detected by lipofuscin and β-galactosidase staining. HE staining showed that the changes of cochlear hair cells, stria vascularis and spiral ganglion cells were obvious in the same group of mice at different ages. Compared with the control group, the aging changes of cochlear hair cells, stria vascularis and spiral ganglion cells were more significant in the experimental group. Immunofluorescence γ-[[H2AX]] staining showed [[H2AX]] phosphorylation in injured cells. The aging of cochlea in mice changed, and staining of β-galactosidase in the experimental group suggested that the striae of blood vessels were changed with age at 32 weeks old and staining of lipofuscin showed dark brown staining around the nucleus (P < 0.05). In conclusion, the deletion of [[RNF8]] is an important cause of morphological changes in the cochlea of mice. The deletion of [[RNF8]] accelerates the aging of the cochlea of mice, suggesting that the apoptosis of the cochlea could contribute to aging in [[RNF8]] gene-deficient mice.
|mesh-terms=* Aging
* Animals
* Apoptosis
* Cochlea
* DNA Damage
* Hair Cells, Auditory
* Histones
* Mice
* Mice, Inbred C57BL
* Spiral Ganglion
* Stria Vascularis
* Ubiquitin-Protein Ligases
|keywords=* DNA damage repair
* RNF8 gene
* aging
* cochlea

}}
{{medline-entry
|title=Function of RAD6B and [[RNF8]] in spermatogenesis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28825854
|abstract=Histone ubiquitination regulates sperm formation and is important for nucleosome removal during spermatogenesis. [[RNF8]] is an E3 ubiquitin ligase, and RAD6B is an E2 ubiquitin-conjugating enzyme. Both proteins participate in DNA damage repair processes via histone ubiquitination. Loss of [[RNF8]] or RAD6B can lead to sterility in male mice. However, the specific mechanisms regulating these ubiquitin-mediated processes are unclear. In this study, we found that [[RNF8]] knockout mice were either subfertile or sterile based on the numbers of offspring they produced. We explored the mechanism by which RAD6B and [[RNF8]] knockouts cause infertility in male mice and compared the effects of their loss on spermatogenesis. Our results demonstrate that RAD6B can polyubiquitinate histones H2 A and H2B. In addition, [[RNF8]] was shown to monoubiquitinate histones H2 A and H2B. Furthermore, we observed that absence of histone ubiquitination was not the only reason for infertility. Senescence played a role in intensifying male sterility by affecting the number of germ cells during spermatogenesis. In summary, both histone ubiquitination and senescence play important roles in spermatogenesis.
|mesh-terms=* Animals
* Cellular Senescence
* Female
* Histones
* Infertility, Male
* Male
* Mice, Knockout
* Protamines
* Seminiferous Tubules
* Spermatids
* Spermatogenesis
* Spermatozoa
* Testis
* Ubiquitin-Conjugating Enzymes
* Ubiquitin-Protein Ligases
* Ubiquitination
|keywords=* RAD6B
* RNF8
* histone
* senescence
* spermatogenesis
* ubiquitin
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884393
}}
{{medline-entry
|title=HTLV-1 Infection and Adult T-Cell Leukemia/Lymphoma-A Tale of Two Proteins: Tax and [[HBZ]].
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27322308
|abstract=HTLV-1 (Human T-cell lymphotropic virus type 1) is a complex human delta retrovirus that currently infects 10-20 million people worldwide. While HTLV-1 infection is generally asymptomatic, 3%-5% of infected individuals develop a highly malignant and intractable T-cell neoplasm known as adult T-cell leukemia/lymphoma (ATL) decades after infection. How HTLV-1 infection progresses to ATL is not well understood. Two viral regulatory proteins, Tax and HTLV-1 basic zipper protein ([[HBZ]]), encoded by the sense and antisense viral transcripts, respectively, are thought to play indispensable roles in the oncogenic process of ATL. This review focuses on the roles of Tax and [[HBZ]] in viral replication, persistence, and oncogenesis. Special emphasis is directed towards recent literature on the mechanisms of action of these two proteins and the roles of Tax and [[HBZ]] in influencing the outcomes of HTLV-1 infection including senescence induction, viral latency and persistence, genome instability, cell proliferation, and ATL development. Attempts are made to integrate results from cell-based studies of HTLV-1 infection and studies of HTLV-1 proviral integration site preference, clonality, and clonal expansion based on high throughput DNA sequencing. Recent data showing that Tax hijacks key mediators of DNA double-strand break repair signaling-the ubiquitin E3 ligase, ring finger protein 8 ([[RNF8]]) and the ubiquitin E2 conjugating enzyme (UBC13)-to activate the canonical nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-κB) and other signaling pathways will be discussed. A perspective on how the Tax-[[RNF8]] signaling axis might impact genomic instability and how Tax may collaborate with [[HBZ]] to drive oncogenesis is provided.
|mesh-terms=* Basic-Leucine Zipper Transcription Factors
* Carcinogenesis
* Gene Products, tax
* Host-Pathogen Interactions
* Human T-lymphotropic virus 1
* Humans
* Leukemia-Lymphoma, Adult T-Cell
* Retroviridae Proteins
* Virus Latency
* Virus Replication
|keywords=* DNA damage response
* HTLV-1
* K63-linked polyubiquitin
* RNF8
* UBC13
* adult T-cell leukemia
* genomic instability
* latency and persistence
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926181
}}