Results 121 to 130 of about 405,671 (296)
Lamina-Associated Domains: Links with Chromosome Architecture, Heterochromatin, and Gene Repression
B. Steensel, A. Belmont
semanticscholar +1 more source
Nonsyndromic orofacial clefts (NSOFCs) are the most common craniofacial defects. Exome sequencing of 214 sporadic cases sheds new light on its genetic architecture and identifies many candidate pathogenic variants. Furthermore, functional studies establish BOC as a novel causal gene and reveal an unusual two‐locus model of inheritance via the epistatic
Qing He+16 more
wiley +1 more source
III. CONTROL BY REPRESSION OF A BIOCHEMICAL PATHWAY [PDF]
Luigi Gorini
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These findings elucidate the innovative role of HIC1 as a transcriptional activator in GC, driving the initiation of pyroptosis and enhancing CD8+ T cell infiltration, which has certain novelty and creative significance. Collectively, targeting HIC1 can present an appealing immunotherapeutic strategy to improve outcomes in GC patients.
Mengjie Kang+4 more
wiley +1 more source
LACTATE-DEGRADING SYSTEM IN BUTYRIBACTERIUM RETTGERI SUBJECT TO GLUCOSE REPRESSION [PDF]
Charles L. Wittenberger, Ann S. Haaf
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A Large Intergenic Noncoding RNA Induced by p53 Mediates Global Gene Repression in the p53 Response
Maite Huarte+14 more
semanticscholar +1 more source
IncRNA‐ZFAS1, an Emerging Gate‐Keeper in DNA Damage‐Dependent Transcriptional Regulation
LncZFAS1 plays a crucial role during DNA damage response in mammalian cells. Loss of lncZFAS1 results in deficient DNA lesion removal and reduced cell viability. Mechanistically, lncZFAS1 modulates RNAPII phosphorylation and transcription and thereby promotes both GG‐NER and TC‐NER upon UV damage.
Jiena Liu+10 more
wiley +1 more source
Induction and Repression by Arginine in Escherichia coli
George W. Forsyth+2 more
openalex +1 more source
Synthesis of Ribonucleic Acid by Human Chromosomes and a Possible Mechanism of its Repression [PDF]
Shigeichi Fujita+3 more
openalex +1 more source
In the context of chronic hyperglycemia, a DDR is initiated, leading to the pathological activation of DNA‐PKcs in the diabetic heart. This activated DNA‐PKcs directly interacts with and phosphorylates YAP1 at Thr226, thereby increasing the nuclear expression of YAP1.
Junyan Wang+10 more
wiley +1 more source