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Erratum.

Autophagy

[No authors listed]
PMID: 26902590
Autophagy. 2016;12(2):443. doi: 10.1080/15548627.2016.1147886.

No abstract available.

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Erratum. Autophagy. 2016;12(2):443doi: 10.1080/15548627.2016.1147886.
(2016). Erratum. Autophagy, 12(2), 443. https://doi.org/10.1080/15548627.2016.1147886
"Erratum." Autophagy vol. 12,2 (2016): 443. doi: https://doi.org/10.1080/15548627.2016.1147886
Erratum. Autophagy. 2016;12(2):443. doi: 10.1080/15548627.2016.1147886. PMID: 26902590; PMCID: PMC4835955.
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Dissection of metabolic reprogramming in polycystic kidney disease reveals coordinated rewiring of bioenergetic pathways.

Communications biology

Podrini C, Rowe I, Pagliarini R, Costa ASH, Chiaravalli M, Di Meo I, Kim H, Distefano G, Tiranti V, Qian F, di Bernardo D, Frezza C, Boletta A.
PMID: 30480096
Commun Biol. 2018 Nov 16;1:194. doi: 10.1038/s42003-018-0200-x. eCollection 2018.

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a genetic disorder caused by loss-of-function mutations in

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Podrini C, Rowe I, Pagliarini R, et al. Dissection of metabolic reprogramming in polycystic kidney disease reveals coordinated rewiring of bioenergetic pathways. Commun Biol. 2018;1:194doi: 10.1038/s42003-018-0200-x.
Podrini, C., Rowe, I., Pagliarini, R., Costa, A. S. H., Chiaravalli, M., Di Meo, I., Kim, H., Distefano, G., Tiranti, V., Qian, F., di Bernardo, D., Frezza, C., & Boletta, A. (2018). Dissection of metabolic reprogramming in polycystic kidney disease reveals coordinated rewiring of bioenergetic pathways. Communications biology, 1194. https://doi.org/10.1038/s42003-018-0200-x
Podrini, Christine, et al. "Dissection of metabolic reprogramming in polycystic kidney disease reveals coordinated rewiring of bioenergetic pathways." Communications biology vol. 1 (2018): 194. doi: https://doi.org/10.1038/s42003-018-0200-x
Podrini C, Rowe I, Pagliarini R, Costa ASH, Chiaravalli M, Di Meo I, Kim H, Distefano G, Tiranti V, Qian F, di Bernardo D, Frezza C, Boletta A. Dissection of metabolic reprogramming in polycystic kidney disease reveals coordinated rewiring of bioenergetic pathways. Commun Biol. 2018 Nov 16;1:194. doi: 10.1038/s42003-018-0200-x. eCollection 2018. PMID: 30480096; PMCID: PMC6240072.
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IL-10-Mediated Refueling of Exhausted T Cell Mitochondria Boosts Anti-Tumour Immunity.

Immunometabolism

Ryan D, Frezza C.
PMID: 34621543
Immunometabolism. 2021 Sep 24;3(4):e210030. doi: 10.20900/immunometab20210030. eCollection 2021 Sep 24.

Immunotherapy has underscored a revolution in cancer treatment. Yet, many patients fail to respond due to T cell exhaustion. Here, an intervention that restores mitochondrial function reversed the exhausted T cell phenotype to promote cytotoxicity and durable anti-tumour responses...

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Ryan D, Frezza C. IL-10-Mediated Refueling of Exhausted T Cell Mitochondria Boosts Anti-Tumour Immunity. Immunometabolism. 2021;3(4):e210030doi: 10.20900/immunometab20210030.
Ryan, D., & Frezza, C. (2021). IL-10-Mediated Refueling of Exhausted T Cell Mitochondria Boosts Anti-Tumour Immunity. Immunometabolism, 3(4), e210030. https://doi.org/10.20900/immunometab20210030
Ryan, Dylan, and Frezza, Christian. "IL-10-Mediated Refueling of Exhausted T Cell Mitochondria Boosts Anti-Tumour Immunity." Immunometabolism vol. 3,4 (2021): e210030. doi: https://doi.org/10.20900/immunometab20210030
Ryan D, Frezza C. IL-10-Mediated Refueling of Exhausted T Cell Mitochondria Boosts Anti-Tumour Immunity. Immunometabolism. 2021 Sep 24;3(4):e210030. doi: 10.20900/immunometab20210030. eCollection 2021 Sep 24. PMID: 34621543; PMCID: PMC7611773.
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Erratum: A three-dimensional engineered tumour for spatial snapshot analysis of cell metabolism and phenotype in hypoxic gradients.

Nature materials

Rodenhizer D, Gaude E, Cojocari D, Mahadevan R, Frezza C, Wouters BG, McGuigan AP.
PMID: 26796735
Nat Mater. 2016 Feb;15(2):244. doi: 10.1038/nmat4515.

No abstract available.

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Rodenhizer D, Gaude E, Cojocari D, et al. Erratum: A three-dimensional engineered tumour for spatial snapshot analysis of cell metabolism and phenotype in hypoxic gradients. Nat Mater. 2016;15(2):244doi: 10.1038/nmat4515.
Rodenhizer, D., Gaude, E., Cojocari, D., Mahadevan, R., Frezza, C., Wouters, B. G., & McGuigan, A. P. (2016). Erratum: A three-dimensional engineered tumour for spatial snapshot analysis of cell metabolism and phenotype in hypoxic gradients. Nature materials, 15(2), 244. https://doi.org/10.1038/nmat4515
Rodenhizer, Darren, et al. "Erratum: A three-dimensional engineered tumour for spatial snapshot analysis of cell metabolism and phenotype in hypoxic gradients." Nature materials vol. 15,2 (2016): 244. doi: https://doi.org/10.1038/nmat4515
Rodenhizer D, Gaude E, Cojocari D, Mahadevan R, Frezza C, Wouters BG, McGuigan AP. Erratum: A three-dimensional engineered tumour for spatial snapshot analysis of cell metabolism and phenotype in hypoxic gradients. Nat Mater. 2016 Feb;15(2):244. doi: 10.1038/nmat4515. PMID: 26796735.
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Targeting Metabolic Plasticity and Flexibility Dynamics for Cancer Therapy.

Cancer discovery

Fendt SM, Frezza C, Erez A.
PMID: 33139243
Cancer Discov. 2020 Dec;10(12):1797-1807. doi: 10.1158/2159-8290.CD-20-0844. Epub 2020 Nov 02.

Cancer cells continuously rewire their metabolism to fulfill their need for rapid growth and survival while subject to changes in environmental cues. Thus, a vital component of a cancer cell lies in its metabolic adaptability. The constant demand for...

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Fendt SM, Frezza C, Erez A. Targeting Metabolic Plasticity and Flexibility Dynamics for Cancer Therapy. Cancer Discov. 2020;10(12):1797-1807doi: 10.1158/2159-8290.CD-20-0844.
Fendt, S. M., Frezza, C., & Erez, A. (2020). Targeting Metabolic Plasticity and Flexibility Dynamics for Cancer Therapy. Cancer discovery, 10(12), 1797-1807. https://doi.org/10.1158/2159-8290.CD-20-0844
Fendt, Sarah-Maria, et al. "Targeting Metabolic Plasticity and Flexibility Dynamics for Cancer Therapy." Cancer discovery vol. 10,12 (2020): 1797-1807. doi: https://doi.org/10.1158/2159-8290.CD-20-0844
Fendt SM, Frezza C, Erez A. Targeting Metabolic Plasticity and Flexibility Dynamics for Cancer Therapy. Cancer Discov. 2020 Dec;10(12):1797-1807. doi: 10.1158/2159-8290.CD-20-0844. Epub 2020 Nov 02. PMID: 33139243; PMCID: PMC7710573.
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Serine Is an Essential Metabolite for Effector T Cell Expansion.

Cell metabolism

Ma EH, Bantug G, Griss T, Condotta S, Johnson RM, Samborska B, Mainolfi N, Suri V, Guak H, Balmer ML, Verway MJ, Raissi TC, Tsui H, Boukhaled G, Henriques da Costa S, Frezza C, Krawczyk CM, Friedman A, Manfredi M, Richer MJ, Hess C, Jones RG.
PMID: 28178570
Cell Metab. 2017 Feb 07;25(2):482. doi: 10.1016/j.cmet.2017.01.014.

No abstract available.

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Ma EH, Bantug G, Griss T, et al. Serine Is an Essential Metabolite for Effector T Cell Expansion. Cell Metab. 2017;25(2):482doi: 10.1016/j.cmet.2017.01.014.
Ma, E. H., Bantug, G., Griss, T., Condotta, S., Johnson, R. M., Samborska, B., Mainolfi, N., Suri, V., Guak, H., Balmer, M. L., Verway, M. J., Raissi, T. C., Tsui, H., Boukhaled, G., Henriques da Costa, S., Frezza, C., Krawczyk, C. M., Friedman, A., Manfredi, M., Richer, M. J., Hess, C., & Jones, R. G. (2017). Serine Is an Essential Metabolite for Effector T Cell Expansion. Cell metabolism, 25(2), 482. https://doi.org/10.1016/j.cmet.2017.01.014
Ma, Eric H, et al. "Serine Is an Essential Metabolite for Effector T Cell Expansion." Cell metabolism vol. 25,2 (2017): 482. doi: https://doi.org/10.1016/j.cmet.2017.01.014
Ma EH, Bantug G, Griss T, Condotta S, Johnson RM, Samborska B, Mainolfi N, Suri V, Guak H, Balmer ML, Verway MJ, Raissi TC, Tsui H, Boukhaled G, Henriques da Costa S, Frezza C, Krawczyk CM, Friedman A, Manfredi M, Richer MJ, Hess C, Jones RG. Serine Is an Essential Metabolite for Effector T Cell Expansion. Cell Metab. 2017 Feb 07;25(2):482. doi: 10.1016/j.cmet.2017.01.014. PMID: 28178570.
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CHCHD4 regulates tumour proliferation and EMT-related phenotypes, through respiratory chain-mediated metabolism.

Cancer & metabolism

Thomas LW, Esposito C, Stephen JM, Costa ASH, Frezza C, Blacker TS, Szabadkai G, Ashcroft M.
PMID: 31346464
Cancer Metab. 2019 Jul 16;7:7. doi: 10.1186/s40170-019-0200-4. eCollection 2019.

BACKGROUND: Mitochondrial oxidative phosphorylation (OXPHOS) via the respiratory chain is required for the maintenance of tumour cell proliferation and regulation of epithelial to mesenchymal transition (EMT)-related phenotypes through mechanisms that are not fully understood. The essential mitochondrial import protein...

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Thomas LW, Esposito C, Stephen JM, et al. CHCHD4 regulates tumour proliferation and EMT-related phenotypes, through respiratory chain-mediated metabolism. Cancer Metab. 2019;7:7doi: 10.1186/s40170-019-0200-4.
Thomas, L. W., Esposito, C., Stephen, J. M., Costa, A. S. H., Frezza, C., Blacker, T. S., Szabadkai, G., & Ashcroft, M. (2019). CHCHD4 regulates tumour proliferation and EMT-related phenotypes, through respiratory chain-mediated metabolism. Cancer & metabolism, 77. https://doi.org/10.1186/s40170-019-0200-4
Thomas, Luke W, et al. "CHCHD4 regulates tumour proliferation and EMT-related phenotypes, through respiratory chain-mediated metabolism." Cancer & metabolism vol. 7 (2019): 7. doi: https://doi.org/10.1186/s40170-019-0200-4
Thomas LW, Esposito C, Stephen JM, Costa ASH, Frezza C, Blacker TS, Szabadkai G, Ashcroft M. CHCHD4 regulates tumour proliferation and EMT-related phenotypes, through respiratory chain-mediated metabolism. Cancer Metab. 2019 Jul 16;7:7. doi: 10.1186/s40170-019-0200-4. eCollection 2019. PMID: 31346464; PMCID: PMC6632184.
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Immunohistochemistry as a tool for screening rare renal cancers.

Annals of translational medicine

Yong C, Stewart GD, Frezza C.
PMID: 31909051
Ann Transl Med. 2019 Dec;7. doi: 10.21037/atm.2019.10.18.

No abstract available.

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Yong C, Stewart GD, Frezza C. Immunohistochemistry as a tool for screening rare renal cancers. Ann Transl Med. 2019;7doi: 10.21037/atm.2019.10.18.
Yong, C., Stewart, G. D., & Frezza, C. (2019). Immunohistochemistry as a tool for screening rare renal cancers. Annals of translational medicine, 7. https://doi.org/10.21037/atm.2019.10.18
Yong, Cissy, et al. "Immunohistochemistry as a tool for screening rare renal cancers." Annals of translational medicine vol. 7 (2019). doi: https://doi.org/10.21037/atm.2019.10.18
Yong C, Stewart GD, Frezza C. Immunohistochemistry as a tool for screening rare renal cancers. Ann Transl Med. 2019 Dec;7. doi: 10.21037/atm.2019.10.18. PMID: 31909051; PMCID: PMC6944496.
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A BAD portion of glucose can be good for inflamed beta cells.

Nature metabolism

Frezza C.
PMID: 32694661
Nat Metab. 2020 May;2(5):383-384. doi: 10.1038/s42255-020-0198-5.

No abstract available.

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Frezza C. A BAD portion of glucose can be good for inflamed beta cells. Nat Metab. 2020;2(5):383-384doi: 10.1038/s42255-020-0198-5.
Frezza, C. (2020). A BAD portion of glucose can be good for inflamed beta cells. Nature metabolism, 2(5), 383-384. https://doi.org/10.1038/s42255-020-0198-5
Frezza, Christian. "A BAD portion of glucose can be good for inflamed beta cells." Nature metabolism vol. 2,5 (2020): 383-384. doi: https://doi.org/10.1038/s42255-020-0198-5
Frezza C. A BAD portion of glucose can be good for inflamed beta cells. Nat Metab. 2020 May;2(5):383-384. doi: 10.1038/s42255-020-0198-5. PMID: 32694661.
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Publisher Correction: A BAD portion of glucose can be good for inflamed beta cells.

Nature metabolism

Frezza C.
PMID: 32694790
Nat Metab. 2020 Jul;2(7):649. doi: 10.1038/s42255-020-0236-3.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Frezza C. Publisher Correction: A BAD portion of glucose can be good for inflamed beta cells. Nat Metab. 2020;2(7):649doi: 10.1038/s42255-020-0236-3.
Frezza, C. (2020). Publisher Correction: A BAD portion of glucose can be good for inflamed beta cells. Nature metabolism, 2(7), 649. https://doi.org/10.1038/s42255-020-0236-3
Frezza, Christian. "Publisher Correction: A BAD portion of glucose can be good for inflamed beta cells." Nature metabolism vol. 2,7 (2020): 649. doi: https://doi.org/10.1038/s42255-020-0236-3
Frezza C. Publisher Correction: A BAD portion of glucose can be good for inflamed beta cells. Nat Metab. 2020 Jul;2(7):649. doi: 10.1038/s42255-020-0236-3. PMID: 32694790; PMCID: PMC7115866.
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Mechanism of succinate efflux upon reperfusion of the ischaemic heart.

Cardiovascular research

Prag HA, Gruszczyk AV, Huang MM, Beach TE, Young T, Tronci L, Nikitopoulou E, Mulvey JF, Ascione R, Hadjihambi A, Shattock MJ, Pellerin L, Saeb-Parsy K, Frezza C, James AM, Krieg T, Murphy MP, Aksentijević D.
PMID: 32766828
Cardiovasc Res. 2021 Mar 21;117(4):1188-1201. doi: 10.1093/cvr/cvaa148.

AIMS: Succinate accumulates several-fold in the ischaemic heart and is then rapidly oxidized upon reperfusion, contributing to reactive oxygen species production by mitochondria. In addition, a significant amount of the accumulated succinate is released from the heart into the...

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Prag HA, Gruszczyk AV, Huang MM, et al. Mechanism of succinate efflux upon reperfusion of the ischaemic heart. Cardiovasc Res. 2021;117(4):1188-1201doi: 10.1093/cvr/cvaa148.
Prag, H. A., Gruszczyk, A. V., Huang, M. M., Beach, T. E., Young, T., Tronci, L., Nikitopoulou, E., Mulvey, J. F., Ascione, R., Hadjihambi, A., Shattock, M. J., Pellerin, L., Saeb-Parsy, K., Frezza, C., James, A. M., Krieg, T., Murphy, M. P., & Aksentijević, D. (2021). Mechanism of succinate efflux upon reperfusion of the ischaemic heart. Cardiovascular research, 117(4), 1188-1201. https://doi.org/10.1093/cvr/cvaa148
Prag, Hiran A, et al. "Mechanism of succinate efflux upon reperfusion of the ischaemic heart." Cardiovascular research vol. 117,4 (2021): 1188-1201. doi: https://doi.org/10.1093/cvr/cvaa148
Prag HA, Gruszczyk AV, Huang MM, Beach TE, Young T, Tronci L, Nikitopoulou E, Mulvey JF, Ascione R, Hadjihambi A, Shattock MJ, Pellerin L, Saeb-Parsy K, Frezza C, James AM, Krieg T, Murphy MP, Aksentijević D. Mechanism of succinate efflux upon reperfusion of the ischaemic heart. Cardiovasc Res. 2021 Mar 21;117(4):1188-1201. doi: 10.1093/cvr/cvaa148. PMID: 32766828; PMCID: PMC7983001.
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