https://transhumanist.ru/index.php?action=history&feed=atom&title=LMNB2 2026-04-08T19:17:09Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=LMNB2&diff=4528&oldid=prev 2021-04-29T19:22:21Z

<p>Новая страница: «Lamin-B2 precursor [LMN2] ==Publications== {{medline-entry |title=Physiological and Pathological Aging Affects Chromatin Dynamics, Structure and Function at the...»</p> <p><b>Новая страница</b></p><div>Lamin-B2 precursor [LMN2]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Physiological and Pathological Aging Affects Chromatin Dynamics, Structure and Function at the Nuclear Edge.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27602048<br /> |abstract=Lamins are intermediate filaments that form a complex meshwork at the inner nuclear membrane. Mammalian cells express two types of Lamins, Lamins A/C and Lamins B, encoded by three different genes, [[LMNA]], [[LMNB1]], and [[LMNB2]]. Mutations in the [[LMNA]] gene are associated with a group of phenotypically diverse diseases referred to as laminopathies. Lamins interact with a large number of binding partners including proteins of the nuclear envelope but also chromatin-associated factors. Lamins not only constitute a scaffold for nuclear shape, rigidity and resistance to stress but also contribute to the organization of chromatin and chromosomal domains. We will discuss here the impact of A-type Lamins loss on alterations of chromatin organization and formation of chromatin domains and how disorganization of the lamina contributes to the patho-physiology of premature aging syndromes. <br /> <br /> |keywords=* Lamins<br /> * epigenetics<br /> * nuclear topology<br /> * premature aging<br /> * telomeres<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993774<br /> }}</div>

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