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Mario Pende

Researcher at French Institute of Health and Medical Research

Publications -  85
Citations -  13210

Mario Pende is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: P70-S6 Kinase 1 & PI3K/AKT/mTOR pathway. The author has an hindex of 43, co-authored 78 publications receiving 11972 citations. Previous affiliations of Mario Pende include Friedrich Miescher Institute for Biomedical Research & Mario Negri Institute for Pharmacological Research.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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S6K1(-/-)/S6K2(-/-) mice exhibit perinatal lethality and rapamycin-sensitive 5'-terminal oligopyrimidine mRNA translation and reveal a mitogen-activated protein kinase-dependent S6 kinase pathway.

Mario Pende, +10 more
- 15 Apr 2004 - 
TL;DR: It is shown that mice deficient for S 6K1 or S6K2 are born at the expected Mendelian ratio, and analysis of S6 phosphorylation in the cytoplasm and nucleoli of cells derived from the distinct S7K genotypes suggests that both kinases are required for full S6osphorylation but that S6k2 may be more prevalent in contributing to this response.
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Disruption of the p70(s6k)/p85(s6k) gene reveals a small mouse phenotype and a new functional S6 kinase.

Hiroshi Shima, +5 more
- 16 Nov 1998 - 
TL;DR: It is demonstrated that homozygous disruption of the p70s 6k/p85s6k gene does not affect viability or fertility of mice, but that it has a significant effect on animal growth, especially during embryogenesis, and the finding of a new S6 kinase gene, which can partly compensate for p70S6k/ p85s 6K function, underscores the importance of S6K function in cell growth.
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The mTOR/PI3K and MAPK pathways converge on eIF4B to control its phosphorylation and activity

David Shahbazian, +9 more
- 21 Jun 2006 - 
TL;DR: It is demonstrated that the p90 ribosomal protein S6 kinase (RSK) phosphorylates eIF4B on the same residue as the S6K and RSK proteins, which increases the interaction of eif4B with the eukaryotic translation initiation factor 3.
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Hypoinsulinaemia, glucose intolerance and diminished beta-cell size in S6K1-deficient mice.

Mario Pende, +8 more
- 21 Dec 2000 - 
TL;DR: It is shown that mice deficient for S6 kinase 1, an effector of the phosphatidylinositide-3-OH kinase signalling pathway, are hypoinsulinaemic and glucose intolerant, which closely parallels those of preclinical type 2 diabetes mellitus, in which malnutrition-induced hypo insulinaemia predisposes individuals to glucose intolerance.