The PERK Eukaryotic Initiation Factor 2α Kinase Is Required for the Development of the Skeletal System, Postnatal Growth, and the Function and Viability of the Pancreas

By Peichuan Zhang, Barbara C. McGrath, Sheng'ai Li, Ami Frank, F. Zambito, Jamie Reinert, M. Gannon, Kun Ma, Kelly McNaughton, D. Cavener. Molecular and Cellular Biology, 2002

637 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Surgery

View Paper: https://www.semanticscholar.org/paper/f14ca4849d71b7803f245de12a1b2066b8cc3da0

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Citations in the corpus

An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. (2003, background): “Two enzymes, Ero1p and Erv2p, have Perk / cells are prone to apoptosis (Harding et al., been identified as proximal oxidases of the yeast ER 2000b, 2001; Zhang et al., 2002), we examined the tem(Frand and Kaiser, 1998; Pollard et al.”
Translation reinitiation at alternative open reading frames regulates gene expression in an integrated stress response (2004, background): “Mutations in specific eIF2 kinases sensitize cells to the cognate stress (Harding et al., 2000b, 2001; Han et al., 2001; Zhang et al., 2002a; Anthony et al., 2004), and mutations that abolish eIF2 phosphorylation altogether, by converting serine 51 to alanine, broadly affect stress resistance (Scheu”
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, positive): “Indeed, this mechanism may be a potential cause of rare forms of juvenile diabetes (Zhang et al., 2002).”
Translational control in the endoplasmic reticulum stress response. (2002, background): “Ultrastructurally, the cells of the affected Perk–/– tissues have characteristic changes in their ER that include the deposition of large quantities of electron-dense material in the lumen (20, 21).”
The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages (2003, background): “In addition, animals harbouring PERK mutations undergo rapid loss of specific secretory cell populations that are exposed to physiologically high levels of endoplasmic reticulum stres”
Initiation and execution of lipotoxic ER stress in pancreatic β-cells (2008, background): “…of the PERK branch, especially in the presence of FFA, leads to β-cell death (Cnop et al., 2007a), whereas mice with deletions of different components of the PERK pathway have progressive β-cell loss and diabetes (Harding et al., 2001; Scheuner et al., 2001; Zhang et al., 2002; Zhang et al., 2006).”
ATF4 is a substrate of RSK2 and an essential regulator of osteoblast biology; implication for Coffin-Lowry Syndrome. (2004, background): “All antibodies tested were purchasedet al., 2000; Harding et al., 2000; Zhang et al., 2002). from Santa Cruz except ATF4-N which was raised against epitopeHowever, PERK deficiency affects other secretory cells QETNKEPPQTVNPIGHLPES.”
Roles of CHOP/GADD153 in endoplasmic reticulum stress (2004, background): “XBP-1 / livers show hypoplasia with numerous apoptotic hepatocytes, and XBP-1 / B cells fail to differentiate to plasma cells.(66,69) PERK / and eIF2a knockin mice have progressive pancreatic b-cell dysfunction due to increased apoptosis of the cells.”
The role for endoplasmic reticulum stress in diabetes mellitus. (2008, background): “Mice with a PERK deletion cannot phosphorylate eIF2 and attenuate insulin translation, and they develop diabetes within a few weeks after birth due to progressive -cell loss (105, 106).”
From acute ER stress to physiological roles of the Unfolded Protein Response (2006, background): “have the same abnormal thinning of bone trabeculae that was observed in ATF4-deficient mice.(74,97) It will be informative to investigate whether tissue-specific knockin of the eIF2a S51A”
Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes (2020, background): “Evidence also indicates that ER stress is essential for β-cell development and survival (Harding et al., 2001; Scheuner et al., 2001; Zhang et al., 2002).”
ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth (2005, background): “Cells with compromised PERK and eIF2a signaling are substantially more sensitive to ER-induced cell death than wild-type cells (Harding et al, 2000b, 2001; Scheuner et al, 2001; Zhang et al, 2002).”