https://transhumanist.ru/index.php?action=history&feed=atom&title=CBX4 2026-04-14T05:18:07Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=CBX4&diff=4578&oldid=prev 2021-04-29T19:24:54Z

<p>Новая страница: «E3 SUMO-protein ligase CBX4 (EC 2.3.2.-) (Chromobox protein homolog 4) (Polycomb 2 homolog) (Pc2) (hPc2) ==Publications== {{medline-entry |title=Biological func...»</p> <p><b>Новая страница</b></p><div>E3 SUMO-protein ligase CBX4 (EC 2.3.2.-) (Chromobox protein homolog 4) (Polycomb 2 homolog) (Pc2) (hPc2)<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Biological functions of chromobox (CBX) proteins in stem cell self-renewal, lineage-commitment, cancer and development.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32979540<br /> |abstract=Epigenetic regulatory proteins support mammalian development, cancer, aging and tissue repair by controlling many cellular processes including stem cell self-renewal, lineage-commitment and senescence in both skeletal and non-skeletal tissues. We review here our knowledge of epigenetic regulatory protein complexes that support the formation of inaccessible heterochromatin and suppress expression of cell and tissue-type specific biomarkers during development. Maintenance and formation of heterochromatin critically depends on epigenetic regulators that recognize histone 3 lysine trimethylation at residues K9 and K27 (respectively, H3K9me3 and H3K27me3), which represent transcriptionally suppressive epigenetic marks. Three chromobox proteins (i.e., [[CBX1]], [[CBX3]] or CBX5) associated with the heterochromatin protein 1 (HP1) complex are methyl readers that interpret H3K9me3 marks which are mediated by H3K9 methyltransferases (i.e., [[SUV39H1]] or SUV39H2). Other chromobox proteins (i.e., [[CBX2]], [[CBX4]], [[CBX6]], [[CBX7]] and CBX8) recognize H3K27me3, which is deposited by Polycomb Repressive Complex 2 (PRC2; a complex containing [[SUZ12]], [[EED]], RBAP46/48 and the methyl transferases [[EZH1]] or EZH2). This second set of CBX proteins resides in [[PRC1]], which has many subunits including other polycomb group factors (PCGF1, [[PCGF2]], [[PCGF3]], PCGF4, [[PCGF5]], PCGF6), human polyhomeotic homologs (HPH1, HPH2, HPH3) and E3-ubiquitin ligases (RING1 or RING2). The latter enzymes catalyze the subsequent mono-ubiquitination of lysine 119 in H2A (H2AK119ub). We discuss biological, cellular and molecular functions of CBX proteins and their physiological and pathological activities in non-skeletal cells and tissues in anticipation of new discoveries on novel roles for CBX proteins in bone formation and skeletal development.<br /> <br /> |keywords=* Aging<br /> * Bone<br /> * CBX1<br /> * CBX2<br /> * CBX3<br /> * CBX4<br /> * CBX5<br /> * CBX6<br /> * CBX7<br /> * CBX8<br /> * Cancer<br /> * Chromatin<br /> * Development<br /> * Epigenetics<br /> * H3K27me3<br /> * H3K9me3<br /> * Lineage-commitment<br /> * Osteoblast<br /> * Senescence<br /> * Stem cell<br /> |full-text-url=https://sci-hub.do/10.1016/j.bone.2020.115659<br /> }}<br /> {{medline-entry<br /> |title=Maintenance of Nucleolar Homeostasis by [[CBX4]] Alleviates Senescence and Osteoarthritis.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30917318<br /> |abstract=[[CBX4]], a component of polycomb repressive complex 1 (PRC1), plays important roles in the maintenance of cell identity and organ development through gene silencing. However, whether [[CBX4]] regulates human stem cell homeostasis remains unclear. Here, we demonstrate that [[CBX4]] counteracts human mesenchymal stem cell (hMSC) aging via the maintenance of nucleolar homeostasis. [[CBX4]] protein is downregulated in aged hMSCs, whereas [[CBX4]] knockout in hMSCs results in destabilized nucleolar heterochromatin, enhanced ribosome biogenesis, increased protein translation, and accelerated cellular senescence. [[CBX4]] maintains nucleolar homeostasis by recruiting nucleolar protein fibrillarin (FBL) and heterochromatin protein KRAB-associated protein 1 (KAP1) at nucleolar rDNA, limiting the excessive expression of rRNAs. Overexpression of [[CBX4]] alleviates physiological hMSC aging and attenuates the development of osteoarthritis in mice. Altogether, our findings reveal a critical role of [[CBX4]] in counteracting cellular senescence by maintaining nucleolar homeostasis, providing a potential therapeutic target for aging-associated disorders.<br /> |mesh-terms=* Animals<br /> * Cell Nucleolus<br /> * Cellular Senescence<br /> * Chromosomal Proteins, Non-Histone<br /> * Gene Knockout Techniques<br /> * Genetic Therapy<br /> * HEK293 Cells<br /> * Homeostasis<br /> * Humans<br /> * Ligases<br /> * Male<br /> * Mesenchymal Stem Cells<br /> * Mice, Inbred C57BL<br /> * Mice, Inbred NOD<br /> * Osteoarthritis<br /> * Polycomb-Group Proteins<br /> |keywords=* CBX4<br /> * CRISPR/Cas9<br /> * aging<br /> * epigenetics<br /> * gene editing<br /> * heterochromatin<br /> * nucleolus<br /> * osteoarthritis<br /> * rDNA<br /> * stem cell<br /> |full-text-url=https://sci-hub.do/10.1016/j.celrep.2019.02.088<br /> }}</div>

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