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2. A homoeostatic switch causing glycerol-3-phosphate and phosphoethanolamine accumulation triggers senescence by rewiring lipid metabolism

4. Cell Metabolic Alterations due to Mcph1 Mutation in Microcephaly

8. Report on three additional patients and genotype–phenotype correlation in SLC25A22-related disorders group

13. Data from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy

14. Supplementary Figures and Methods from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy

15. Table S2 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy

16. Key Resources Table from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy

21. Supplementary data from In Vivo Detection of Succinate by Magnetic Resonance Spectroscopy as a Hallmark of SDHx Mutations in Paraganglioma

24. Relevance of the TRIAP1/p53 axis in colon cancer cell proliferation and adaptation to glutamine deprivation

25. Cyanide resistant respiration and the alternative oxidase pathway : A from to mammals

29. SDH Mutations Establish a Hypermethylator Phenotype in Paraganglioma

31. Defects in succinate dehydrogenase in gastrointestinal stromal tumors lacking KIT and PDGFRA mutations

32. Expression of the yeast NADH dehydrogenase Ndi1 in Drosophila confers increased lifespan independently of dietary restriction

37. Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy

47. Germline mutations in FH confer predisposition to malignant pheochromocytomas and paragangliomas

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