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TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis.

Molecular cell

Pan JA, Sun Y, Jiang YP, Bott AJ, Jaber N, Dou Z, Yang B, Chen JS, Catanzaro JM, Du C, Ding WX, Diaz-Meco MT, Moscat J, Ozato K, Lin RZ, Zong WX.
PMID: 27058791
Mol Cell. 2016 Apr 07;62(1):149-51. doi: 10.1016/j.molcel.2016.03.015.

No abstract available.

Cite
Pan JA, Sun Y, Jiang YP, et al. TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis. Mol Cell. 2016;62(1):149-51doi: 10.1016/j.molcel.2016.03.015.
Pan, J. A., Sun, Y., Jiang, Y. P., Bott, A. J., Jaber, N., Dou, Z., Yang, B., Chen, J. S., Catanzaro, J. M., Du, C., Ding, W. X., Diaz-Meco, M. T., Moscat, J., Ozato, K., Lin, R. Z., & Zong, W. X. (2016). TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis. Molecular cell, 62(1), 149-51. https://doi.org/10.1016/j.molcel.2016.03.015
Pan, Ji-An, et al. "TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis." Molecular cell vol. 62,1 (2016): 149-51. doi: https://doi.org/10.1016/j.molcel.2016.03.015
Pan JA, Sun Y, Jiang YP, Bott AJ, Jaber N, Dou Z, Yang B, Chen JS, Catanzaro JM, Du C, Ding WX, Diaz-Meco MT, Moscat J, Ozato K, Lin RZ, Zong WX. TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis. Mol Cell. 2016 Apr 07;62(1):149-51. doi: 10.1016/j.molcel.2016.03.015. PMID: 27058791.
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An Orthotopic Implantation Mouse Model of Hepatocellular Carcinoma with Underlying Liver Steatosis.

STAR protocols

Kasashima H, Duran A, Cid-Diaz T, Kudo Y, Diaz-Meco MT, Moscat J.
PMID: 33377079
STAR Protoc. 2020 Nov 20;1(3):100185. doi: 10.1016/j.xpro.2020.100185. eCollection 2020 Dec 18.

This protocol provides the steps required for a mouse liver orthotopic implantation model. The reliable pre-clinical animal models that have similar characteristics to hepatocellular carcinoma (HCC) are a powerful tool to unveil the mechanisms controlling tumor initiation and progression....

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Kasashima H, Duran A, Cid-Diaz T, et al. An Orthotopic Implantation Mouse Model of Hepatocellular Carcinoma with Underlying Liver Steatosis. STAR Protoc. 2020;1(3):100185doi: 10.1016/j.xpro.2020.100185.
Kasashima, H., Duran, A., Cid-Diaz, T., Kudo, Y., Diaz-Meco, M. T., & Moscat, J. (2020). An Orthotopic Implantation Mouse Model of Hepatocellular Carcinoma with Underlying Liver Steatosis. STAR protocols, 1(3), 100185. https://doi.org/10.1016/j.xpro.2020.100185
Kasashima, Hiroaki, et al. "An Orthotopic Implantation Mouse Model of Hepatocellular Carcinoma with Underlying Liver Steatosis." STAR protocols vol. 1,3 (2020): 100185. doi: https://doi.org/10.1016/j.xpro.2020.100185
Kasashima H, Duran A, Cid-Diaz T, Kudo Y, Diaz-Meco MT, Moscat J. An Orthotopic Implantation Mouse Model of Hepatocellular Carcinoma with Underlying Liver Steatosis. STAR Protoc. 2020 Nov 20;1(3):100185. doi: 10.1016/j.xpro.2020.100185. eCollection 2020 Dec 18. PMID: 33377079; PMCID: PMC7757567.
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Correction for Linares et al., "Phosphorylation of p62 by cdk1 Controls the Timely Transit of Cells through Mitosis and Tumor Cell Proliferation".

Molecular and cellular biology

Linares JF, Amanchy R, Greis K, Diaz-Meco MT, Moscat J.
PMID: 28710122
Mol Cell Biol. 2017 Jul 14;37(15). doi: 10.1128/MCB.00252-17. Print 2017 Aug 01.

No abstract available.

Cite
Linares JF, Amanchy R, Greis K, et al. Correction for Linares et al., "Phosphorylation of p62 by cdk1 Controls the Timely Transit of Cells through Mitosis and Tumor Cell Proliferation". Mol Cell Biol. 2017;37(15)doi: 10.1128/MCB.00252-17.
Linares, J. F., Amanchy, R., Greis, K., Diaz-Meco, M. T., & Moscat, J. (2017). Correction for Linares et al., "Phosphorylation of p62 by cdk1 Controls the Timely Transit of Cells through Mitosis and Tumor Cell Proliferation". Molecular and cellular biology, 37(15), . https://doi.org/10.1128/MCB.00252-17
Linares, Juan F, et al. "Correction for Linares et al., "Phosphorylation of p62 by cdk1 Controls the Timely Transit of Cells through Mitosis and Tumor Cell Proliferation"." Molecular and cellular biology vol. 37,15 (2017). doi: https://doi.org/10.1128/MCB.00252-17
Linares JF, Amanchy R, Greis K, Diaz-Meco MT, Moscat J. Correction for Linares et al., "Phosphorylation of p62 by cdk1 Controls the Timely Transit of Cells through Mitosis and Tumor Cell Proliferation". Mol Cell Biol. 2017 Jul 14;37(15). doi: 10.1128/MCB.00252-17. Print 2017 Aug 01. PMID: 28710122; PMCID: PMC5514453.
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Repression of Intestinal Stem Cell Function and Tumorigenesis through Direct Phosphorylation of β-Catenin and Yap by PKCζ.

Cell reports

Llado V, Nakanishi Y, Duran A, Reina-Campos M, Shelton PM, Linares JF, Yajima T, Campos A, Aza-Blanc P, Leitges M, Diaz-Meco MT, Moscat J.
PMID: 25660024
Cell Rep. 2015 Feb 10;10(5):740-754. doi: 10.1016/j.celrep.2015.01.007. Epub 2015 Feb 05.

Intestinal epithelial homeostasis requires continuous renewal supported by stem cells located in the base of the crypt. Disruption of this balance results in failure to regenerate and initiates tumorigenesis. The β-catenin and Yap pathways in Lgr5

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Llado V, Nakanishi Y, Duran A, et al. Repression of Intestinal Stem Cell Function and Tumorigenesis through Direct Phosphorylation of β-Catenin and Yap by PKCζ. Cell Rep. 2015;10(5):740-754doi: 10.1016/j.celrep.2015.01.007.
Llado, V., Nakanishi, Y., Duran, A., Reina-Campos, M., Shelton, P. M., Linares, J. F., Yajima, T., Campos, A., Aza-Blanc, P., Leitges, M., Diaz-Meco, M. T., & Moscat, J. (2015). Repression of Intestinal Stem Cell Function and Tumorigenesis through Direct Phosphorylation of β-Catenin and Yap by PKCζ. Cell reports, 10(5), 740-754. https://doi.org/10.1016/j.celrep.2015.01.007
Llado, Victoria, et al. "Repression of Intestinal Stem Cell Function and Tumorigenesis through Direct Phosphorylation of β-Catenin and Yap by PKCζ." Cell reports vol. 10,5 (2015): 740-754. doi: https://doi.org/10.1016/j.celrep.2015.01.007
Llado V, Nakanishi Y, Duran A, Reina-Campos M, Shelton PM, Linares JF, Yajima T, Campos A, Aza-Blanc P, Leitges M, Diaz-Meco MT, Moscat J. Repression of Intestinal Stem Cell Function and Tumorigenesis through Direct Phosphorylation of β-Catenin and Yap by PKCζ. Cell Rep. 2015 Feb 10;10(5):740-754. doi: 10.1016/j.celrep.2015.01.007. Epub 2015 Feb 05. PMID: 25660024; PMCID: PMC4524805.
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Role of adipose and hepatic atypical protein kinase C lambda (PKCλ) in the development of obesity and glucose intolerance.

Adipocyte

Habegger KM, Matzke D, Ottaway N, Hembree J, Holland J, Raver C, Mansfeld J, Müller TD, Perez-Tilve D, Pfluger PT, Lee SJ, Diaz-Meco M, Moscat J, Leitges M, Tschöp MH, Hofmann SM.
PMID: 23700535
Adipocyte. 2012 Oct 01;1(4):203-214. doi: 10.4161/adip.20891.

PKCλ, an atypical member of the multifunctional protein kinase C family, has been implicated in the regulation of insulin-stimulated glucose transport and of the intracellular immune response. To further elucidate the role of this cellular regulator in diet-induced obesity...

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Habegger KM, Matzke D, Ottaway N, et al. Role of adipose and hepatic atypical protein kinase C lambda (PKCλ) in the development of obesity and glucose intolerance. Adipocyte. 2012;1(4):203-214doi: 10.4161/adip.20891.
Habegger, K. M., Matzke, D., Ottaway, N., Hembree, J., Holland, J., Raver, C., Mansfeld, J., Müller, T. D., Perez-Tilve, D., Pfluger, P. T., Lee, S. J., Diaz-Meco, M., Moscat, J., Leitges, M., Tschöp, M. H., & Hofmann, S. M. (2012). Role of adipose and hepatic atypical protein kinase C lambda (PKCλ) in the development of obesity and glucose intolerance. Adipocyte, 1(4), 203-214. https://doi.org/10.4161/adip.20891
Habegger, Kirk M, et al. "Role of adipose and hepatic atypical protein kinase C lambda (PKCλ) in the development of obesity and glucose intolerance." Adipocyte vol. 1,4 (2012): 203-214. doi: https://doi.org/10.4161/adip.20891
Habegger KM, Matzke D, Ottaway N, Hembree J, Holland J, Raver C, Mansfeld J, Müller TD, Perez-Tilve D, Pfluger PT, Lee SJ, Diaz-Meco M, Moscat J, Leitges M, Tschöp MH, Hofmann SM. Role of adipose and hepatic atypical protein kinase C lambda (PKCλ) in the development of obesity and glucose intolerance. Adipocyte. 2012 Oct 01;1(4):203-214. doi: 10.4161/adip.20891. PMID: 23700535; PMCID: PMC3609106.
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Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm.

Autophagy

Moscat J, Cuervo AM, Diaz-Meco MT.
PMID: 34895031
Autophagy. 2021 Dec 12;1-2. doi: 10.1080/15548627.2021.1991192. Epub 2021 Dec 12.

The mechanisms controlling immunosurveillance and immunoevasion often operate simultaneously to the triggering of the oncogenic signaling that results in tumor initiation. The resolution of the balance between anti-cancer immune responses and pro-tumorigenic pathways determines if a tumor cell survives...

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Moscat J, Cuervo AM, Diaz-Meco MT. Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm. Autophagy. 2021;1-2doi: 10.1080/15548627.2021.1991192.
Moscat, J., Cuervo, A. M., & Diaz-Meco, M. T. (2021). Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm. Autophagy, 1-2. https://doi.org/10.1080/15548627.2021.1991192
Moscat, Jorge, et al. "Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm." Autophagy vol. (2021): 1-2. doi: https://doi.org/10.1080/15548627.2021.1991192
Moscat J, Cuervo AM, Diaz-Meco MT. Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm. Autophagy. 2021 Dec 12;1-2. doi: 10.1080/15548627.2021.1991192. Epub 2021 Dec 12. PMID: 34895031.
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PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis.

Molecular cell

Linares JF, Zhang X, Martinez-Ordoñez A, Duran A, Kinoshita H, Kasashima H, Nakanishi N, Nakanishi Y, Carelli R, Cappelli L, Arias E, Yashiro M, Ohira M, Patel S, Inghirami G, Loda M, Cuervo AM, Diaz-Meco MT, Moscat J.
PMID: 34560002
Mol Cell. 2021 Nov 04;81(21):4509-4526.e10. doi: 10.1016/j.molcel.2021.08.039. Epub 2021 Sep 23.

The interferon (IFN) pathway is critical for cytotoxic T cell activation, which is central to tumor immunosurveillance and successful immunotherapy. We demonstrate here that PKCλ/ι inactivation results in the hyper-stimulation of the IFN cascade and the enhanced recruitment of...

Cite
Linares JF, Zhang X, Martinez-Ordoñez A, et al. PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis. Mol Cell. 2021;81(21):4509-4526.e10doi: 10.1016/j.molcel.2021.08.039.
Linares, J. F., Zhang, X., Martinez-Ordoñez, A., Duran, A., Kinoshita, H., Kasashima, H., Nakanishi, N., Nakanishi, Y., Carelli, R., Cappelli, L., Arias, E., Yashiro, M., Ohira, M., Patel, S., Inghirami, G., Loda, M., Cuervo, A. M., Diaz-Meco, M. T., & Moscat, J. (2021). PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis. Molecular cell, 81(21), 4509-4526.e10. https://doi.org/10.1016/j.molcel.2021.08.039
Linares, Juan F, et al. "PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis." Molecular cell vol. 81,21 (2021): 4509-4526.e10. doi: https://doi.org/10.1016/j.molcel.2021.08.039
Linares JF, Zhang X, Martinez-Ordoñez A, Duran A, Kinoshita H, Kasashima H, Nakanishi N, Nakanishi Y, Carelli R, Cappelli L, Arias E, Yashiro M, Ohira M, Patel S, Inghirami G, Loda M, Cuervo AM, Diaz-Meco MT, Moscat J. PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis. Mol Cell. 2021 Nov 04;81(21):4509-4526.e10. doi: 10.1016/j.molcel.2021.08.039. Epub 2021 Sep 23. PMID: 34560002; PMCID: PMC8571054.
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Nutrient stress revamps cancer cell metabolism.

Cell research

Moscat J, Richardson A, Diaz-Meco MT.
PMID: 25828529
Cell Res. 2015 May;25(5):537-8. doi: 10.1038/cr.2015.38. Epub 2015 Mar 31.

Efforts to identify new therapeutic targets in cancer primarily focused on oncogenes and tumor suppressor genes, and their mechanisms of action. However, there is an emerging alternative strategy that involves identification of target proteins that are not encoded by...

Cite
Moscat J, Richardson A, Diaz-Meco MT. Nutrient stress revamps cancer cell metabolism. Cell Res. 2015;25(5):537-8doi: 10.1038/cr.2015.38.
Moscat, J., Richardson, A., & Diaz-Meco, M. T. (2015). Nutrient stress revamps cancer cell metabolism. Cell research, 25(5), 537-8. https://doi.org/10.1038/cr.2015.38
Moscat, Jorge, et al. "Nutrient stress revamps cancer cell metabolism." Cell research vol. 25,5 (2015): 537-8. doi: https://doi.org/10.1038/cr.2015.38
Moscat J, Richardson A, Diaz-Meco MT. Nutrient stress revamps cancer cell metabolism. Cell Res. 2015 May;25(5):537-8. doi: 10.1038/cr.2015.38. Epub 2015 Mar 31. PMID: 25828529; PMCID: PMC4423079.
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Correction: p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote Tumorigenesis.

Cancer research

Lam HC, Baglini CV, Lope AL, Parkhitko AA, Liu HJ, Alesi N, Malinowska IA, Ebrahimi-Fakhari D, Saffari A, Yu JJ, Pereira A, Khabibullin D, Ogorek B, Nijmeh J, Kavanagh T, Handen A, Chan SY, Asara JM, Oldham WM, Diaz-Meco MT, Moscat J, Sahin M, Priolo C, Henske EP.
PMID: 33268556
Cancer Res. 2020 Dec 01;80(23):5424. doi: 10.1158/0008-5472.CAN-20-3417.

No abstract available.

Cite
Lam HC, Baglini CV, Lope AL, et al. Correction: p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote Tumorigenesis. Cancer Res. 2020;80(23):5424doi: 10.1158/0008-5472.CAN-20-3417.
Lam, H. C., Baglini, C. V., Lope, A. L., Parkhitko, A. A., Liu, H. J., Alesi, N., Malinowska, I. A., Ebrahimi-Fakhari, D., Saffari, A., Yu, J. J., Pereira, A., Khabibullin, D., Ogorek, B., Nijmeh, J., Kavanagh, T., Handen, A., Chan, S. Y., Asara, J. M., Oldham, W. M., Diaz-Meco, M. T., Moscat, J., Sahin, M., Priolo, C., & Henske, E. P. (2020). Correction: p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote Tumorigenesis. Cancer research, 80(23), 5424. https://doi.org/10.1158/0008-5472.CAN-20-3417
Lam, Hilaire C, et al. "Correction: p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote Tumorigenesis." Cancer research vol. 80,23 (2020): 5424. doi: https://doi.org/10.1158/0008-5472.CAN-20-3417
Lam HC, Baglini CV, Lope AL, Parkhitko AA, Liu HJ, Alesi N, Malinowska IA, Ebrahimi-Fakhari D, Saffari A, Yu JJ, Pereira A, Khabibullin D, Ogorek B, Nijmeh J, Kavanagh T, Handen A, Chan SY, Asara JM, Oldham WM, Diaz-Meco MT, Moscat J, Sahin M, Priolo C, Henske EP. Correction: p62/SQSTM1 Cooperates with Hyperactive mTORC1 to Regulate Glutathione Production, Maintain Mitochondrial Integrity, and Promote Tumorigenesis. Cancer Res. 2020 Dec 01;80(23):5424. doi: 10.1158/0008-5472.CAN-20-3417. PMID: 33268556.
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Mouse model of colorectal cancer: orthotopic co-implantation of tumor and stroma cells in cecum and rectum.

STAR protocols

Kasashima H, Duran A, Cid-Diaz T, Muta Y, Kinoshita H, Batlle E, Diaz-Meco MT, Moscat J.
PMID: 33554135
STAR Protoc. 2021 Jan 22;2(1):100297. doi: 10.1016/j.xpro.2021.100297. eCollection 2021 Mar 19.

No abstract available.

Cite
Kasashima H, Duran A, Cid-Diaz T, et al. Mouse model of colorectal cancer: orthotopic co-implantation of tumor and stroma cells in cecum and rectum. STAR Protoc. 2021;2(1):100297doi: 10.1016/j.xpro.2021.100297.
Kasashima, H., Duran, A., Cid-Diaz, T., Muta, Y., Kinoshita, H., Batlle, E., Diaz-Meco, M. T., & Moscat, J. (2021). Mouse model of colorectal cancer: orthotopic co-implantation of tumor and stroma cells in cecum and rectum. STAR protocols, 2(1), 100297. https://doi.org/10.1016/j.xpro.2021.100297
Kasashima, Hiroaki, et al. "Mouse model of colorectal cancer: orthotopic co-implantation of tumor and stroma cells in cecum and rectum." STAR protocols vol. 2,1 (2021): 100297. doi: https://doi.org/10.1016/j.xpro.2021.100297
Kasashima H, Duran A, Cid-Diaz T, Muta Y, Kinoshita H, Batlle E, Diaz-Meco MT, Moscat J. Mouse model of colorectal cancer: orthotopic co-implantation of tumor and stroma cells in cecum and rectum. STAR Protoc. 2021 Jan 22;2(1):100297. doi: 10.1016/j.xpro.2021.100297. eCollection 2021 Mar 19. PMID: 33554135; PMCID: PMC7843928.
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PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis.

Molecular cell

Linares JF, Zhang X, Martinez-Ordoñez A, Duran A, Kinoshita H, Kasashima H, Nakanishi N, Nakanishi Y, Carelli R, Cappelli L, Arias E, Yashiro M, Ohira M, Patel S, Inghirami G, Loda M, Cuervo AM, Diaz-Meco MT, Moscat J.
PMID: 34560002
Mol Cell. 2021 Nov 04;81(21):4509-4526.e10. doi: 10.1016/j.molcel.2021.08.039. Epub 2021 Sep 23.

The interferon (IFN) pathway is critical for cytotoxic T cell activation, which is central to tumor immunosurveillance and successful immunotherapy. We demonstrate here that PKCλ/ι inactivation results in the hyper-stimulation of the IFN cascade and the enhanced recruitment of...

Cite
Linares JF, Zhang X, Martinez-Ordoñez A, et al. PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis. Mol Cell. 2021;81(21):4509-4526.e10doi: 10.1016/j.molcel.2021.08.039.
Linares, J. F., Zhang, X., Martinez-Ordoñez, A., Duran, A., Kinoshita, H., Kasashima, H., Nakanishi, N., Nakanishi, Y., Carelli, R., Cappelli, L., Arias, E., Yashiro, M., Ohira, M., Patel, S., Inghirami, G., Loda, M., Cuervo, A. M., Diaz-Meco, M. T., & Moscat, J. (2021). PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis. Molecular cell, 81(21), 4509-4526.e10. https://doi.org/10.1016/j.molcel.2021.08.039
Linares, Juan F, et al. "PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis." Molecular cell vol. 81,21 (2021): 4509-4526.e10. doi: https://doi.org/10.1016/j.molcel.2021.08.039
Linares JF, Zhang X, Martinez-Ordoñez A, Duran A, Kinoshita H, Kasashima H, Nakanishi N, Nakanishi Y, Carelli R, Cappelli L, Arias E, Yashiro M, Ohira M, Patel S, Inghirami G, Loda M, Cuervo AM, Diaz-Meco MT, Moscat J. PKCλ/ι inhibition activates an ULK2-mediated interferon response to repress tumorigenesis. Mol Cell. 2021 Nov 04;81(21):4509-4526.e10. doi: 10.1016/j.molcel.2021.08.039. Epub 2021 Sep 23. PMID: 34560002; PMCID: PMC8571054.
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