Results 121 to 130 of about 16,717 (221)
Xist condensates: perspectives for therapeutic intervention
Genome BiologyAbstract X-chromosome inactivation (XCI) is a crucial mechanism of dosage compensation in female mammals ensuring that genes from only one X chromosome are expressed, initiated through expression of the long noncoding RNA Xist. Recent evidence underscores the significance of molecular crowding—most likely via liquid–liquid phase separation ...
Perotti, Irene +3 more
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Developmental Xist Induction is Mediated by Enhanced Splicing [PDF]
, 2019 Dosage compensation in female placental animals is accomplished by silencing one of the two X-chromosomes. X-chromosome inactivation (XCI) is initiated early in development by preferentially upregulating the lncRNA Xist expression from the future ...
Stork, Cheryl Anne
core
XIST and MUC1-C form an auto-regulatory pathway in driving cancer progression
Cell Death and DiseaseThe long non-coding RNA X-inactive specific transcript (lncRNA XIST) and MUC1 gene are dysregulated in chronic inflammation and cancer; however, there is no known interaction of their functions.
Keyi Wang +8 more
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Non-Coding RNABackground/Objectives: X-inactive-specific transcript (XIST) is a factor that plays a role in neuroinflammation. This study investigated the role of XIST in neuronal development, neuroinflammation, myelination, and therapeutic responses within cerebral ...
Nihan Aktas Pepe +4 more
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The damage signal is displayed by addition of a H2AX mark, recognized by Tp53bp1 and E3 ligases Rnf8 and Rnf168, in addition to MDC1, XRCC5 and XRCC6, and DNA-PKc, whereupon it is transduced to BRCA1 along with Rad family genes, as well all ATM/ATR and CHEK1/2.
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LncRNA XIST promotes bladder cancer progression by modulating miR-129-5p/TNFSF10 axis
Discover OncologyBackground The differential expression, biological function, and ceRNA regulatory mechanism of lncRNA XIST in bladder cancer (BC) were investigated, and its clinical values for the early diagnosis of bladder cancer patients were elucidated.
Yu-Lin Kong +4 more
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We provide a brief summary of studies from our laboratory that establish Xist activation or repression by impairment or loss of tumor suppressor function, control of Xist by DNA damage and repair pathways, establish the Xist non-coding RNA as an epigenetic modulator of autosomal gene expression, identify the existence of an Xist RNP complex that ...
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We measured total transcription in cells in concert with N1-methyladenosine (m1A) profiling, in cells with intact Albkh3 and in cells lacking Alkbh3. We report here interaction of the non-coding RNA Xist with Alkbh3.
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