Results 201 to 210 of about 376,518 (330)

Lactylation‐Driven YTHDC1 Alleviates MASLD by Suppressing PTPN22‐Mediated Dephosphorylation of NLRP3

open access: yesAdvanced Science, EarlyView.
In MASLD, YTHDC1 undergoes increased lactylation and ubiquitination, reducing its expression. AARS1 mediates lactylation at lysine 565, while disrupted binding to LDHA further promotes lactylation, suppressing YTHDC1. This downregulation enhances PTPN22 mRNA stability, leading to NLRP3 dephosphorylation and activation, which exacerbates inflammation ...
Feng Zhang   +16 more
wiley   +1 more source

The splicing factor PTBP1 interacts with RUNX1 and is required for leukemia cell survival. [PDF]

open access: yesLeukemia
Dhir A   +12 more
europepmc   +1 more source

Dysregulation of CircZNF79(5) Modulates YBX1 Stability and Selective Autophagy to Drive Hepatocellular Carcinoma Progression

open access: yesAdvanced Science, EarlyView.
In HCC, circZNF79(5) binds to YBX1 and functions as an oncogene, recruits BRCC36 to remove K63‐linked ubiquitin chains to stabilize YBX1 protein, and promotes HCC progression via the HIF‐1 signaling pathway. Conversely, circZNF79(5) silencing activates the AMPK/mTOR pathway, inducing p62‐mediated selective autophagic degradation of YBX1.
Xueqiang Guo   +20 more
wiley   +1 more source

Skeletal Muscle HSF1 Alleviates Age‐Associated Sarcopenia and Mitochondrial Function Decline via SIRT3‐PGC1α Axis

open access: yesAdvanced Science, EarlyView.
Aged HSF1 muscle‐specific knockout mice show deteriorated muscle atrophy and metabolic dysfunction, while active HSF1 overexpression improves muscle function via activating SIRT3 to deacetylate both PGC1α1 and PGC1α4, which boosts mitochondrial function and muscle hypertrophy in a fiber‐type specific manner, and induces FNDC5/Irisin for tissue ...
Jun Zhang   +18 more
wiley   +1 more source

Splicing factor Sf3b1 facilitates maintenance of neuronal dendrites by modulating mitochondrial health. [PDF]

open access: yesCell Mol Life Sci
Tsao WC   +6 more
europepmc   +1 more source

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