FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W228798924> ?p ?o ?g. }

• W228798924 endingPage "e0126768" @default.
• W228798924 startingPage "e0126768" @default.
• W228798924 abstract "The immunoproteasome is upregulated by disease, oxidative stress, and inflammatory cytokines, suggesting an expanded role for the immunoproteasome in stress signaling that goes beyond its canonical role in generating peptides for antigen presentation. The signaling pathways that are regulated by the immunoproteasome remain elusive. However, previous studies suggest a role for the immunoproteasome in the regulation of PTEN and NF-κB signaling. One well-known pathway upstream of NF-κB and downstream of PTEN is the Akt signaling pathway, which is responsible for mediating cellular survival and is modulated after optic nerve crush (ONC). This study investigated the role of retinal immunoproteasome after injury induced by ONC, focusing on the Akt cell survival pathway. Retinas or retinal pigment epithelial (RPE) cells from wild type (WT) and knockout (KO) mice lacking either one (LMP2) or two (LMP7 and MECL-1) catalytic subunits of the immunoproteasome were utilized in this study. We show that mRNA and protein levels of the immunoproteasome subunits are significantly upregulated in WT retinas following ONC. Mice lacking the immunoproteasome subunits show either a delayed or dampened apoptotic response as well as altered Akt signaling, compared to WT mice after ONC. Treatment of the RPE cells with insulin growth factor-1 (IGF-1) to stimulate Akt signaling confirmed that the immunoproteasome modulates this pathway, and most likely modulates parallel pathways as well. This study links the inducible expression of the immunoproteasome following retinal injury to Akt signaling, which is important in many disease pathways." @default.
• W228798924 created "2016-06-24" @default.
• W228798924 creator A5001825366 @default.
• W228798924 creator A5018568966 @default.
• W228798924 creator A5019854999 @default.
• W228798924 creator A5028545189 @default.
• W228798924 creator A5035222785 @default.
• W228798924 creator A5038626370 @default.
• W228798924 creator A5071049390 @default.
• W228798924 creator A5076869038 @default.
• W228798924 creator A5084610227 @default.
• W228798924 creator A5088177487 @default.
• W228798924 date "2015-05-15" @default.
• W228798924 modified "2023-09-26" @default.
• W228798924 title "Immunoproteasome Deficiency Protects in the Retina after Optic Nerve Crush" @default.
• W228798924 cites W1471166809 @default.
• W228798924 cites W1481321944 @default.
• W228798924 cites W1640850494 @default.
• W228798924 cites W1884132335 @default.
• W228798924 cites W1893444436 @default.
• W228798924 cites W1906407967 @default.
• W228798924 cites W1966217447 @default.
• W228798924 cites W1966667280 @default.
• W228798924 cites W1968659926 @default.
• W228798924 cites W1971430693 @default.
• W228798924 cites W1972621679 @default.
• W228798924 cites W1974010669 @default.
• W228798924 cites W1980845575 @default.
• W228798924 cites W1982178335 @default.
• W228798924 cites W1987011447 @default.
• W228798924 cites W1987092078 @default.
• W228798924 cites W1991343786 @default.
• W228798924 cites W1993705148 @default.
• W228798924 cites W1995641301 @default.
• W228798924 cites W1995805772 @default.
• W228798924 cites W2000091638 @default.
• W228798924 cites W2000383792 @default.
• W228798924 cites W2004538934 @default.
• W228798924 cites W2008744347 @default.
• W228798924 cites W2010247968 @default.
• W228798924 cites W2010352524 @default.
• W228798924 cites W2011863717 @default.
• W228798924 cites W2012262387 @default.
• W228798924 cites W2012441394 @default.
• W228798924 cites W2019055460 @default.
• W228798924 cites W2019478598 @default.
• W228798924 cites W2023366550 @default.
• W228798924 cites W2027575720 @default.
• W228798924 cites W2035101626 @default.
• W228798924 cites W2036356274 @default.
• W228798924 cites W2037038463 @default.
• W228798924 cites W2042991032 @default.
• W228798924 cites W2056513212 @default.
• W228798924 cites W2058045644 @default.
• W228798924 cites W2060582345 @default.
• W228798924 cites W2062301537 @default.
• W228798924 cites W2063508296 @default.
• W228798924 cites W2065902811 @default.
• W228798924 cites W2067910590 @default.
• W228798924 cites W2069720095 @default.
• W228798924 cites W2069723920 @default.
• W228798924 cites W2070434454 @default.
• W228798924 cites W2074797041 @default.
• W228798924 cites W2075732775 @default.
• W228798924 cites W2078114300 @default.
• W228798924 cites W2078318856 @default.
• W228798924 cites W2080683593 @default.
• W228798924 cites W2084304228 @default.
• W228798924 cites W2084843323 @default.
• W228798924 cites W2086357515 @default.
• W228798924 cites W2087087295 @default.
• W228798924 cites W2087473057 @default.
• W228798924 cites W2094166578 @default.
• W228798924 cites W2102683915 @default.
• W228798924 cites W2108393782 @default.
• W228798924 cites W2112495348 @default.
• W228798924 cites W2117397120 @default.
• W228798924 cites W2127202058 @default.
• W228798924 cites W2134421329 @default.
• W228798924 cites W2135288413 @default.
• W228798924 cites W2140103571 @default.
• W228798924 cites W2141420900 @default.
• W228798924 cites W2157579823 @default.
• W228798924 cites W2159049015 @default.
• W228798924 cites W2164028372 @default.
• W228798924 cites W2168875502 @default.
• W228798924 cites W2346624188 @default.
• W228798924 cites W4231865486 @default.
• W228798924 cites W4245438556 @default.
• W228798924 doi "https://doi.org/10.1371/journal.pone.0126768" @default.
• W228798924 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4433222" @default.
• W228798924 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25978061" @default.
• W228798924 hasPublicationYear "2015" @default.
• W228798924 type Work @default.
• W228798924 sameAs 228798924 @default.
• W228798924 citedByCount "13" @default.
• W228798924 countsByYear W2287989242016 @default.
• W228798924 countsByYear W2287989242017 @default.

• next