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1957 1
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1961 3
1962 4
1963 3
1964 5
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1966 3
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1968 7
1969 1
1970 1
1971 4
1972 3
1973 4
1974 6
1975 7
1976 1
1977 3
1978 6
1979 6
1980 5
1981 5
1982 5
1983 11
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1986 7
1987 7
1988 11
1989 4
1990 13
1991 6
1992 5
1993 6
1994 6
1995 5
1996 7
1997 5
1998 5
1999 10
2000 18
2001 43
2002 65
2003 86
2004 103
2005 146
2006 182
2007 211
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2011 416
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The following term was not found in PubMed: Luitze
Page 1
Trimethylamine N-Oxide Binds and Activates PERK to Promote Metabolic Dysfunction.
Chen S, Henderson A, Petriello MC, Romano KA, Gearing M, Miao J, Schell M, Sandoval-Espinola WJ, Tao J, Sha B, Graham M, Crooke R, Kleinridders A, Balskus EP, Rey FE, Morris AJ, Biddinger SB. Chen S, et al. Cell Metab. 2019 Dec 3;30(6):1141-1151.e5. doi: 10.1016/j.cmet.2019.08.021. Epub 2019 Sep 19. Cell Metab. 2019. PMID: 31543404 Free article.
The mechanism by which TMAO promotes disease is unclear. We now reveal the endoplasmic reticulum stress kinase PERK (EIF2AK3) as a receptor for TMAO: TMAO binds to PERK at physiologically relevant concentrations; selectively activates the PERK branch of the u …
The mechanism by which TMAO promotes disease is unclear. We now reveal the endoplasmic reticulum stress kinase PERK (EIF2AK3) as a re …
Ablation of the endoplasmic reticulum stress kinase PERK induces paraptosis and type I interferon to promote anti-tumor T cell responses.
Mandula JK, Chang S, Mohamed E, Jimenez R, Sierra-Mondragon RA, Chang DC, Obermayer AN, Moran-Segura CM, Das S, Vazquez-Martinez JA, Prieto K, Chen A, Smalley KSM, Czerniecki B, Forsyth P, Koya RC, Ruffell B, Cubillos-Ruiz JR, Munn DH, Shaw TI, Conejo-Garcia JR, Rodriguez PC. Mandula JK, et al. Cancer Cell. 2022 Oct 10;40(10):1145-1160.e9. doi: 10.1016/j.ccell.2022.08.016. Epub 2022 Sep 22. Cancer Cell. 2022. PMID: 36150390 Free PMC article.
Here, we investigate the role of the UPR mediator pancreatic ER kinase (PKR)-like ER kinase (PERK) in cancer cells in the modulation of anti-tumor immunity. Deletion of PERK in cancer cells or pharmacological inhibition of PERK in melanoma-bearing mice incite …
Here, we investigate the role of the UPR mediator pancreatic ER kinase (PKR)-like ER kinase (PERK) in cancer cells in the modulation …
The PERKs of mitochondria protection during stress: insights for PERK modulation in neurodegenerative and metabolic diseases.
Almeida LM, Pinho BR, Duchen MR, Oliveira JMA. Almeida LM, et al. Biol Rev Camb Philos Soc. 2022 Oct;97(5):1737-1748. doi: 10.1111/brv.12860. Epub 2022 Apr 26. Biol Rev Camb Philos Soc. 2022. PMID: 35475315 Review.
The location of PERK at the contact sites between the ER and the mitochondria creates a PERK-mitochondria axis that allows PERK to detect stress in both organelles, adapt their functions and prevent apoptosis. ...But how does PERK mediate all these cha …
The location of PERK at the contact sites between the ER and the mitochondria creates a PERK-mitochondria axis that allows …
PERK controls bone homeostasis through the regulation of osteoclast differentiation and function.
Guo J, Ren R, Sun K, Yao X, Lin J, Wang G, Guo Z, Xu T, Guo F. Guo J, et al. Cell Death Dis. 2020 Oct 13;11(10):847. doi: 10.1038/s41419-020-03046-z. Cell Death Dis. 2020. PMID: 33051453 Free PMC article.
Systemic PERK knockout mice show severe bone loss, suggesting that PERK is of great significance for maintaining the normal growth and development of bone tissue, but the role of PERK in osteoclastogenesis is still unclear. In this study, we found that PER …
Systemic PERK knockout mice show severe bone loss, suggesting that PERK is of great significance for maintaining the normal gr …
The endoplasmic reticulum kinase PERK interacts with the oxidoreductase ERO1 to metabolically adapt mitochondria.
Bassot A, Chen J, Takahashi-Yamashiro K, Yap MC, Gibhardt CS, Le GNT, Hario S, Nasu Y, Moore J, Gutiérrez T, Mina L, Mast H, Moses A, Bhat R, Ballanyi K, Lemieux H, Sitia R, Zito E, Bogeski I, Campbell RE, Simmen T. Bassot A, et al. Cell Rep. 2023 Jan 31;42(1):111899. doi: 10.1016/j.celrep.2022.111899. Epub 2022 Dec 30. Cell Rep. 2023. PMID: 36586409 Free article.
We now show that the oxidoreductase ERO1 covalently interacts with protein kinase RNA-like ER kinase (PERK) upon treatment with tunicamycin. The PERK-ERO1 interaction requires the C-terminal active site of ERO1 and cysteine 216 of PERK. Moreover, we show that …
We now show that the oxidoreductase ERO1 covalently interacts with protein kinase RNA-like ER kinase (PERK) upon treatment with tunic …
Loss of PERK function promotes ferroptosis by downregulating SLC7A11 (System Xc-) in colorectal cancer.
Saini KK, Chaturvedi P, Sinha A, Singh MP, Khan MA, Verma A, Nengroo MA, Satrusal SR, Meena S, Singh A, Srivastava S, Sarkar J, Datta D. Saini KK, et al. Redox Biol. 2023 Sep;65:102833. doi: 10.1016/j.redox.2023.102833. Epub 2023 Jul 28. Redox Biol. 2023. PMID: 37536085 Free PMC article.
PERK inhibition reduces ATF4 expression and recruitment to the promoter of SLC7A11 and results in its downregulation. ...Further, by performing TCGA data mining and using colorectal cancer patient samples, we demonstrate that the expression of PERK and SLC7A11 is po …
PERK inhibition reduces ATF4 expression and recruitment to the promoter of SLC7A11 and results in its downregulation. ...Further, by …
PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress.
Verfaillie T, Rubio N, Garg AD, Bultynck G, Rizzuto R, Decuypere JP, Piette J, Linehan C, Gupta S, Samali A, Agostinis P. Verfaillie T, et al. Cell Death Differ. 2012 Nov;19(11):1880-91. doi: 10.1038/cdd.2012.74. Epub 2012 Jun 15. Cell Death Differ. 2012. PMID: 22705852 Free PMC article.
PERK(-/-) cells display disturbed ER morphology and Ca(2+) signaling as well as significantly weaker ER-mitochondria contact sites. Re-expression of a kinase-dead PERK mutant but not the cytoplasmic deletion mutant of PERK in PERK(-/-) cells re-establi …
PERK(-/-) cells display disturbed ER morphology and Ca(2+) signaling as well as significantly weaker ER-mitochondria contact sites. R …
Mfn2 Regulates High Glucose-Induced MAMs Dysfunction and Apoptosis in Podocytes via PERK Pathway.
Cao Y, Chen Z, Hu J, Feng J, Zhu Z, Fan Y, Lin Q, Ding G. Cao Y, et al. Front Cell Dev Biol. 2021 Dec 20;9:769213. doi: 10.3389/fcell.2021.769213. eCollection 2021. Front Cell Dev Biol. 2021. PMID: 34988075 Free PMC article.
Mfn2 physically interacts with PERK, and HG promotes a decrease in Mfn2-PERK interaction. In addition, Mfn2-silenced podocytes showed mitochondrial dysfunction, MAMs reduction, activation of PERK pathway, and increased apoptosis. ...Therefore, this study conf …
Mfn2 physically interacts with PERK, and HG promotes a decrease in Mfn2-PERK interaction. In addition, Mfn2-silenced podocytes …
Pharmacologic Activation of a Compensatory Integrated Stress Response Kinase Promotes Mitochondrial Remodeling in PERK-deficient Cells.
Perea V, Baron KR, Dolina V, Aviles G, Rosarda JD, Guo X, Kampmann M, Wiseman RL. Perea V, et al. bioRxiv [Preprint]. 2023 May 17:2023.03.11.532186. doi: 10.1101/2023.03.11.532186. bioRxiv. 2023. PMID: 36945406 Free PMC article. Updated. Preprint.
Deficiencies in PERK signaling lead to mitochondrial dysfunction and contribute to the pathogenesis of numerous diseases. We define the potential for pharmacologic activation of compensatory eIF2alpha kinases to rescue ISR signaling and promote mitochondrial adaptation in …
Deficiencies in PERK signaling lead to mitochondrial dysfunction and contribute to the pathogenesis of numerous diseases. We define t …
Endothelial PERK-ATF4-JAG1 axis activated by T-ALL remodels bone marrow vascular niche.
Liu C, Chen Q, Shang Y, Chen L, Myers J, Awadallah A, Sun J, Yu S, Umphred-Wilson K, Che D, Dou Y, Li L, Wearsch P, Ramírez-Bergeron D, Beck R, Xin W, Jin G, Adoro S, Zhou L. Liu C, et al. Theranostics. 2022 Mar 21;12(6):2894-2907. doi: 10.7150/thno.67710. eCollection 2022. Theranostics. 2022. PMID: 35401837 Free PMC article.
Methods: in this study, we assessed the transcriptomic and phenotypic alterations in UPR response of the bone marrow endothelial cells (ECs) in mice engrafted with T-ALL and in bone marrow specimens from patients who have T-ALL. We used PERK inhibitor and generated endothe …
Methods: in this study, we assessed the transcriptomic and phenotypic alterations in UPR response of the bone marrow endothelial cells (ECs) …
10,958 results
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