Редактирование: DDB1

DNA damage-binding protein 1 (DDB p127 subunit) (DNA damage-binding protein a) (DDBa) (Damage-specific DNA-binding protein 1) (HBV X-associated protein 1) (XAP-1) (UV-damaged DNA-binding factor) (UV-damaged DNA-binding protein 1) (UV-DDB 1) (XPE-binding factor) (XPE-BF) (Xeroderma pigmentosum group E-complementing protein) (XPCe) [XAP1]

==Publications==

{{medline-entry
|title=DCAF1 regulates Treg senescence via the ROS axis during immunological aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32730228
|abstract=As a hallmark of immunological aging, low-grade, chronic inflammation with accumulation of effector memory T cells contributes to increased susceptibility to many aging-related diseases. While the proinflammatory state of aged T cells indicates a dysregulation of immune homeostasis, whether and how aging drives regulatory T cell (Treg) aging and alters Treg function are not fully understood owing to a lack of specific aging markers. Here, by a combination of cellular, molecular, and bioinformatic approaches, we discovered that Tregs senesce more severely than conventional T (Tconv) cells during aging. We found that Tregs from aged mice were less efficient than young Tregs in suppressing Tconv cell function in an inflammatory bowel disease model and in preventing Tconv cell aging in an irradiation-induced aging model. Furthermore, we revealed that [[DDB1]]- and CUL4-associated factor 1 (DCAF1) was downregulated in aged Tregs and was critical to restrain Treg aging via reactive oxygen species (ROS) regulated by glutathione-S-transferase P ([[GSTP1]]). Importantly, interfering with [[GSTP1]] and ROS pathways reinvigorated the proliferation and function of aged Tregs. Therefore, our studies uncover an important role of the DCAF1/[[GSTP1]]/ROS axis in Treg senescence, which leads to uncontrolled inflammation and immunological aging.

|keywords=* Aging
* Cellular senescence
* Immunology
* Inflammatory bowel disease
* T cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7598062
}}
{{medline-entry
|title=Deletion of [[DDB1]]- and CUL4- associated factor-17 (Dcaf17) gene causes spermatogenesis defects and male infertility in mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29907856
|abstract=[[DDB1]]- and CUL4-associated factor 17 (Dcaf17) is a member of DCAF family genes that encode substrate receptor proteins for Cullin-RING E3 ubiquitin ligases, which play critical roles in many cellular processes. To unravel the function of [[DCAF17]], we performed expression profiling of Dcaf17 in different tissues of wild type mouse by qRT-PCR and generated Dcaf17 knockout mice by gene targeting. Expression profiling of Dcaf17 showed highest expression in testis. Analyses of Dcaf17 transcripts during post-natal development of testis at different ages displayed gradual increase in Dcaf17 mRNA levels with the age. Although Dcaf17 disruption did not have any effect on female fertility, Dcaf17 deletion led to male infertility due to abnormal sperm development. The Dcaf17   mice produced low number of sperm with abnormal shape and significantly low motility. Histological examination of the Dcaf17   testis revealed impaired spermatogenesis with presence of vacuoles and sloughed cells in the seminiferous tubules. Disruption of Dcaf17 caused asymmetric acrosome capping, impaired nuclear compaction and abnormal round spermatid to elongated spermatid transition. For the first time, these data indicate that [[DCAF17]] is essential for spermiogenesis.
|mesh-terms=* Aging
* Animals
* Gene Deletion
* Infertility, Male
* Male
* Mice
* Mice, Knockout
* Seminiferous Tubules
* Sperm Motility
* Spermatids
* Spermatogenesis
* Ubiquitin-Protein Ligase Complexes

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6003934
}}
{{medline-entry
|title=Accelerated protein evolution analysis reveals genes and pathways associated with the evolution of mammalian longevity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22205409
|abstract=The genetic basis of the large species differences in longevity and aging remains a mystery. Thanks to recent large-scale genome sequencing efforts, the genomes of multiple species have been sequenced and can be used for cross-species comparisons to study species divergence in longevity. By analyzing proteins under accelerated evolution in several mammalian lineages where maximum lifespan increased, we identified genes and processes that are candidate targets of selection when longevity evolves. We identified several proteins with longevity-specific selection patterns, including [[COL3A1]] that has previously been related to aging and proteins related to DNA damage repair and response such as [[DDB1]] and [[CAPNS1]]. Moreover, we found that processes such as lipid metabolism and cholesterol catabolism show such patterns of selection and suggest a link between the evolution of lipid metabolism, cholesterol catabolism, and the evolution of longevity. Lastly, we found evidence that the proteasome-ubiquitin system is under selection specific to lineages where longevity increased and suggest that its selection had a role in the evolution of longevity. These results provide evidence that natural selection acts on species when longevity evolves, give insights into adaptive genetic changes associated with the evolution of longevity in mammals, and provide evidence that at least some repair systems are selected for when longevity increases.
|mesh-terms=* Aging
* Animals
* Genomics
* Humans
* Longevity
* Mammals
* Phylogeny
* Proteins
* Selection, Genetic

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3592953
}}