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Table representation of search results timeline featuring number of search results per year.

Year Number of Results
1945 1
1946 1
1947 3
1948 1
1950 1
1951 2
1956 1
1957 1
1958 1
1961 3
1962 4
1963 3
1964 5
1965 2
1966 3
1967 1
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
1984 7
1985 9
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 212
2008 248
2009 283
2010 345
2011 416
2012 486
2013 591
2014 625
2015 713
2016 764
2017 827
2018 878
2019 936
2020 998
2021 1024
2022 528
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Search Results

9,428 results
Results by year
Filters applied: . Clear all 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 …
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 PERK-EIF2α-ATF4 signaling branch regulates osteoblast differentiation and proliferation by PTH.
Zhang K, Wang M, Li Y, Li C, Tang S, Qu X, Feng N, Wu Y. Zhang K, et al. Am J Physiol Endocrinol Metab. 2019 Apr 1;316(4):E590-E604. doi: 10.1152/ajpendo.00371.2018. Epub 2019 Jan 22. Am J Physiol Endocrinol Metab. 2019. PMID: 30668150 Free article.
Furthermore, we observed that PTH increased the association between heat shock protein 90 (HSP90) and PERK and maintained PERK protein stabilization in the early stages of PTH-induced ER stress. Treatment of MC3T3-E1 cells with geldanamycin, an HSP90 inhibitor, decr …
Furthermore, we observed that PTH increased the association between heat shock protein 90 (HSP90) and PERK and maintained PERK
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 modulates the UPR and mitochondrial function via repression of PERK.
Muñoz JP, Ivanova S, Sánchez-Wandelmer J, Martínez-Cristóbal P, Noguera E, Sancho A, Díaz-Ramos A, Hernández-Alvarez MI, Sebastián D, Mauvezin C, Palacín M, Zorzano A. Muñoz JP, et al. EMBO J. 2013 Aug 28;32(17):2348-61. doi: 10.1038/emboj.2013.168. Epub 2013 Aug 6. EMBO J. 2013. PMID: 23921556 Free PMC article.
Silencing of PERK increased the apoptosis of Mfn2-ablated cells in response to ER stress. ...In summary, our data indicate that Mfn2 is an upstream modulator of PERK. Furthermore, Mfn2 loss-of-function reveals that PERK is a key regulator of mitochondrial mor …
Silencing of PERK increased the apoptosis of Mfn2-ablated cells in response to ER stress. ...In summary, our data indicate that Mfn2 …
The Unfolded Protein Response: An Overview.
Read A, Schröder M. Read A, et al. Biology (Basel). 2021 Apr 29;10(5):384. doi: 10.3390/biology10050384. Biology (Basel). 2021. PMID: 33946669 Free PMC article. Review.
The activation of the UPR involves three signaling pathways, IRE1, PERK and ATF6, which all play vital roles in returning protein homeostasis to levels seen in non-stressed cells. ...This pathway involves spliceosome independent splicing of HAC1 or XBP1 in yeast and mammal …
The activation of the UPR involves three signaling pathways, IRE1, PERK and ATF6, which all play vital roles in returning protein hom …
PERK mediates oxidative stress and adipogenesis in Graves' orbitopathy pathogenesis.
Ko J, Kim JY, Kyoung Chae M, Jig Lee E, Sook Yoon J. Ko J, et al. J Mol Endocrinol. 2021 May 11;66(4):313-323. doi: 10.1530/JME-21-0057. J Mol Endocrinol. 2021. PMID: 33870911
PERK silencing inhibited CSE- or hydrogen peroxide-induced ROS generation. ...Our results imply that PERK-modulating agents can potentially be used to manage GO....
PERK silencing inhibited CSE- or hydrogen peroxide-induced ROS generation. ...Our results imply that PERK-modulating agents ca
The ER Stress Sensor PERK Coordinates ER-Plasma Membrane Contact Site Formation through Interaction with Filamin-A and F-Actin Remodeling.
van Vliet AR, Giordano F, Gerlo S, Segura I, Van Eygen S, Molenberghs G, Rocha S, Houcine A, Derua R, Verfaillie T, Vangindertael J, De Keersmaecker H, Waelkens E, Tavernier J, Hofkens J, Annaert W, Carmeliet P, Samali A, Mizuno H, Agostinis P. van Vliet AR, et al. Mol Cell. 2017 Mar 2;65(5):885-899.e6. doi: 10.1016/j.molcel.2017.01.020. Epub 2017 Feb 23. Mol Cell. 2017. PMID: 28238652 Free article.
Here, using proximity-dependent biotin identification (BioID), we identified the actin-binding protein Filamin A (FLNA) as a key PERK interactor. Cells lacking PERK accumulate F-actin at the cell edges and display reduced ER-PM contacts. ...Cytosolic Ca(2+) elevatio …
Here, using proximity-dependent biotin identification (BioID), we identified the actin-binding protein Filamin A (FLNA) as a key PERK
The Role of PERK in Understanding Development of Neurodegenerative Diseases.
Smedley GD, Walker KE, Yuan SH. Smedley GD, et al. Int J Mol Sci. 2021 Jul 29;22(15):8146. doi: 10.3390/ijms22158146. Int J Mol Sci. 2021. PMID: 34360909 Free PMC article. Review.
Genetic and clinical studies show a correlation between failure of the PERK pathway in neural cells and the development of neurodegeneration, but the wide array of methodology of these studies is presenting conflicting narratives about the role of PERK in these affe …
Genetic and clinical studies show a correlation between failure of the PERK pathway in neural cells and the development of neurodegen …
PERK signaling pathway in bone metabolism: Friend or foe?
Guo J, Ren R, Sun K, He J, Shao J. Guo J, et al. Cell Prolif. 2021 Apr;54(4):e13011. doi: 10.1111/cpr.13011. Epub 2021 Feb 21. Cell Prolif. 2021. PMID: 33615575 Free PMC article. Review.
The double-stranded RNA-dependent protein kinase (PKR)-like ER kinase (PERK) is a key transmembrane protein that regulates ER stress, and growing evidence suggests that the PERK pathway plays a crucial role in regulating bone metabolism under both physiological and …
The double-stranded RNA-dependent protein kinase (PKR)-like ER kinase (PERK) is a key transmembrane protein that regulates ER stress, …
9,428 results