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Targeting the BCKDK/BCLAF1/MYC/HK2 axis to alter aerobic glycolysis and overcome Trametinib resistance in lung cancer

ABSTRACT: BCKDK is a branched-chain amino acid metabolizing enzyme whose expression is up-regulated in tumors. BCKDK is closely associated with the development, progression, and metastasis of a wide range of tumors; however, the mechanisms behind this association remain poorly understood. To explore the pro-tumorigenic molecular mechanism of BCKDK, we performed RNA sequencing analysis of BCKDK-deficient H1299 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE269486 | GEO | 2025/05/25

REPOSITORIES: GEO

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Targeting the BCKDK/BCLAF1/MYC/HK2 axis to alter aerobic glycolysis and overcome Trametinib resistance in lung cancer

Project description:Targeting the BCKDK/BCLAF1/MYC/HK2 axis to alter aerobic glycolysis and overcome Trametinib resistance in lung cancer

| PRJNA1122131 | ENA

CRISPR-RfxCas13d screening uncovers Bckdk as a post-translational regulator of the maternal-to-zygotic transition in teleosts [CUT&Run]

Project description:The Maternal-to-Zygotic transition (MZT) is a reprograming process encompassing zygotic genome activation (ZGA) and the clearance of maternally-provided mRNAs. While some factors regulating MZT have been identified, there are thousands of maternal RNAs whose function has not been ascribed yet. Here, we have performed a proof-of-principle CRISPR-RfxCas13d maternal screening targeting mRNAs encoding protein kinases and phosphatases in zebrafish and identified Bckdk as a novel post-translational regulator of MZT. Bckdk mRNA knockdown caused epiboly defects, ZGA deregulation, H3K27ac reduction and a partial impairment of miR-430 processing. Phospho-proteomic analysis revealed that Phf10 (Baf45a), a chromatin remodeling factor, is less phosphorylated upon Bckdk depletion. Further, phf10 mRNA knockdown also altered ZGA and Phf10 constitutively phosphorylated rescued the developmental defects after bckdk mRNA depletion. Altogether, our results demonstrate the competence of CRISPR-RfxCas13d screenings to uncover new regulators of early vertebrate development and shed light on the post-translational control of MZT mediated by protein phosphorylation.

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CRISPR-RfxCas13d screening uncovers Bckdk as a post-translational regulator of the maternal-to-zygotic transition in teleosts [RNA ppp4r2a_phf10]

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CRISPR-RfxCas13d screening uncovers Bckdk as a post-translational regulator of the maternal-to-zygotic transition in teleosts [RNA Medaka]

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CRISPR-RfxCas13d screening uncovers Bckdk as a post-translational regulator of the maternal-to-zygotic transition in teleosts [RNA-Seq rescue]

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Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy

Project description:Autism is present in 1% of the population, yet treatments are extremely limited. We identified homozygous inactivating mutations in the BCKDK gene in families presenting with autism and epilepsy. The encoded branched chain ketoacid dehydrogenase kinase protein is responsible for phosphorylation-mediated inactivation of the E1-alpha subunit of branched chain ketoacid dehydrogenase, itself mutated in Maple Syrup Urine Disease (MSUD). Patients with homozygous BCKDK mutations display reductions in BCKDK mRNA and protein, E1-alpha phosphorylation and serum branched chain amino acids (BCAAs). Bckdk knockout mice show abnormal brain amino acids profiles and neurobehavioral defects, which are largely corrected by dietary BCAA supplementation. Thus autism presenting with epilepsy due to BCKDK mutations represent a new and potentially treatable disease. A 51 chip study that includes both human and mouse samples to investigate the expression changes that result in a mutation or knockout of the BCKDK gene. Starting with human fibroblasts from three affecteds and two controls, cells were converted into IPSs, then NPCs, and finally Neurons. Each of these cell types were used to view the expression changes between a cells with a BCKDK mutation versus controls. Finally, a mouse knockout was performed to verify consistency of the expression pattern differences between the BCKCK knockout and wild-type. Samples are labeled as Affected if the sample came from a patient with a BCKDK mutation and WildType otherwise. Samples were usually replicated once.

2012-07-17 | E-GEOD-39447 | biostudies-arrayexpress

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