HoldsUp

Guido Kroemer

University of Paris Descartes

Guido Kroemer is a professor at the University of Paris Descartes specializing in immunology, cancer biology, aging, and autophagy. His research investigates mechanisms of regulated cell death, including apoptosis, ferroptosis, and immunogenic cell death. His publications also explore cancer immunotherapy, gut microbiota interventions in oncology, and therapeutic targets in metabolic and age-related diseases.

38 claims checked on air: 3 context 1 contradicted 2 overstated 28 supported 4 unverified 3 flagged

What they said on air - unverified

0:07:15unverifiedvery lowDr. Guido Kroemer on Autophagy, Caloric Restriction Mimetics

Acetyltransferases have a low affinity for acetyl-CoA compared to kinases' affinity for ATP, making protein acetylation highly sensitive to fluctuations in acetyl-CoA levels whereas phosphorylation is relatively insensitive to ATP fluctuations.

"acetyltransferases are having a low affinity for acetyl-CoA as compared to kinases, which have a high affinity for ATP. So if you vary the ATP concentration in the cell, it has little impact on phosphorylation reactions. But if you vary acetyl concentration, it has a major impact on the acetylation level of cellular proteins." (said at 0:07:15)

No published record matching the claim that acetyltransferases have a lower affinity for acetyl-CoA compared to kinases' affinity for ATP—rendering protein acetylation sensitive to acetyl-CoA fluctuations while phosphorylation remains relatively insensitive to ATP fluctuations—was located; this does not prove the claim false.

0:11:53unverifiedvery lowDr. Guido Kroemer on Autophagy, Caloric Restriction Mimetics

Autophagy can be pharmacologically induced via a cell-permeable Beclin-1-activating peptide or via mTOR inhibitors without inducing protein deacetylation.

"when you induce autophagy by pharmacological tricks such as a cell-permeable peptide that dissociates an inhibitory interaction between a Golgi protein and Beclin-1, you can induce autophagy without that protein deacetylation would occur before. And similarly, when you give chemical inhibitors of mTOR like rapamycin or the rapalogs, there's also no protein deacetylation." (said at 0:11:53)

No published record matching the claim that autophagy can be pharmacologically induced via a cell-permeable Beclin-1-activating peptide or via mTOR inhibitors without inducing protein deacetylation was located; this does not prove the claim false.

0:17:50unverifiedvery lowDr. Guido Kroemer on Autophagy, Caloric Restriction Mimetics

In humans, fasting for 3 to 4 days is required to observe robust induction of autophagy in circulating leukocytes.

"what we did on circulating leukocytes is that we needed to wait for 3 or 4 days to see massive induction of autophagy." (said at 0:17:50)

No published record matching the specific claim that 3 to 4 days of fasting is required to observe robust or massive induction of autophagy in human circulating leukocytes was located; this does not prove the claim false. While shorter-term fasting and exercise-induced fasting protocols have been studied for their effects on autophagic markers in human tissues and peripheral blood mononuclear cells, specific empirical publications defining a strict 3- to 4-day requirement for leukocyte autophagy induction were not identified in the indexed literature.

0:59:51unverifiedvery lowDr. Guido Kroemer on Autophagy, Caloric Restriction Mimetics

Combining an acetyltransferase inhibitor and a deacetylase activator produces a synergistic effect on autophagy in mice.

"inhibiting the acetyltransferase and activating the deacetylase will have, of course, a synergistic effect. ... Well, you can show this in mice" (said at 0:59:51)

No published record matching the claim that combining an acetyltransferase inhibitor and a deacetylase activator produces a synergistic effect on autophagy in mice was located; this does not prove the claim false.

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