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    Cieśla et al. delineate an N6-methyladenosine (m6A)-dependent translational circuitry directing wild-type SF3B1 synthesis and ensuing splicing of DNA repair and epigenetic factors upon oncogenic stress. SF3B1 translation control counteracts genotoxic stress in malignant hematopoietic precursor cells, highlighting a conserved role for m6A/SF3B1-driven splicing regulation in myelodysplastic…

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    • New study linking RNA epitranscriptomic, translation control and splicing in leukemia. @CieslaMaciej @BellodiCristian & co-authors @MolecularCell #AACR23 https://t.co/H8TKPsvwpN

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    Paget et al. report that stress granules, condensates that form on cellular stresses, are involved in antiviral innate immunity. Stress granules prevent excessive innate immune activation to protect cells from immune-mediated cell death in viral infections and auto-immunopathology diseases. This suggests a function for SGs to maintain cellular homeostasis.

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    • RT @MolecularCell: Stress granules are shock absorbers that prevent excessive innate immune responses to dsRNA https://t.co/w69Rl8NQDl

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    Mitochondria engage both feedback and feedforward control circuits to achieve the robust regulation of metabolism. A diverse array of molecular sensors monitors metabolite levels and fine-tunes enzymatic activities, ensuring swift adaptation to metabolic demand and effective protection against stress.

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    • Metabolic sensing and control in mitochondria https://t.co/NNI1BBfRga

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    The cis-regulatory code dictates how DNA sequence controls quantitative transcription levels of each gene depending on cellular context. Kim and Wysocka review progress and challenges in understanding the layers of this code, from transcription factor binding to cofactor recruitment and ultimately cis-regulatory element specificity and function within complex regulatory landscapes.

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    • Deciphering the multi-scale, quantitative cis-regulatory code https://t.co/nSRcnUzqWd #trancscription #enhancers #chromatin #nuclearorganization #generegulation FOUR LAYERS OF THE CIS- REGULATORY CODE: https://t.co/mwKaFwqgm6

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    Ghosh et al. report that the tumor suppressor, TP53, activates the innate immune response to suppress tumor growth. TP53 promotes the degradation of the cytosolic DNA exonuclease TREX1, resulting in cytoplasmic DNA accumulation and activation of the cGAS/STING pathway. The absence of cGAS or STING compromises p53’s tumor suppressor activity.

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    • RT @MolecularCell: Online Now: p53 engages the cGAS/STING cytosolic DNA sensing pathway for tumor suppression https://t.co/CiiVhdNqeG

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    Ghosh et al. report that the tumor suppressor, TP53, activates the innate immune response to suppress tumor growth. TP53 promotes the degradation of the cytosolic DNA exonuclease TREX1, resulting in cytoplasmic DNA accumulation and activation of the cGAS/STING pathway. The absence of cGAS or STING compromises p53’s tumor suppressor activity.

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    • RT @ivanoamelio: p53 engages the cGAS/STING cytosolic DNA sensing pathway for tumor suppression: Molecular Cell https://t.co/bCeJ3mp1JQ

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    Bomber et al. utilize degron tagging of the endogenous human chromatin-remodeling enzyme SMARCA5, coupled with a multi-omics approach, to define the requirements for SMARCA5-mediated nucleosome sliding. SMARCA5 co-localized with H2A.Z and CTCF and was required for CTCF DNA binding, nucleosomal phasing at these sites, and maintaining nucleosome repeat length.

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    • RT @MolecularCell: Online Now: Human SMARCA5 is continuously required to maintain nucleosome spacing https://t.co/IELMCqFwqv