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In vitro arsenic exposure increased SQSTM1 and UNKL expression and decreased SPSB1 transcript stability in human fibroblasts (Qiu et al.
MicroRNA Samples Diseases Target Effects on CD UC autophagy miR-142-3p * HCT116 + - ATG16L1, Inhibit NOD2 miR-320 HT-29 + + NOD2, Inhibit NF-[kappa]B miR-192 * HCT116 + - NOD2, Inhibit NF-[kappa]B miR-122 HT-29 + - NOD2, Inhibit NF-[kappa]B miR-93; Human colon + - ATG16L1 Inhibit miR-106B tissues, HCT116 PTEN miR-30C; Human intestinal + - ATG5, Inhibit miR-130a epithelial T84 ATG16L1 cells/mice mTOR enterocytes miR-346 Human intestinal + + Vitamin D Upregulate epithelial cells receptor (VDR) GSK3B miR-20a Human colonic + - BECN1, Inhibit mucosal tissues ATG16L1, SQSTM1 MiR-196 * Human epithelial + - LC3-II, Inhibit cells IRGM miR-665 Human/mice + + XBP1, Induce colonic mucosal ORMDL3 tissues.
The p62/sequestosome 1 (SQSTM1) protein acts as a cargo receptor for autophagic degradation of ubiquitinated targets.
(11.) Rios M, Langston AL, Alonso N, Goodman K, Selby PL, Fraser WD, et al, Mutation of SQSTM1 are associated with severity and clinical outcome in Paget's disease of bone.
These four loci--sites in the genes PLA2G2C, SQSTM1, SLC4A4, and IGH--had not previously been associated with arsenic exposure.
In addition to apoptosis, multiple forms of regulated cell death exist, such as autophagic cell death that is associated with lipidation of microtubuleassociated protein light chain 3 (LC3) and degradation of sequestosome 1 (SQSTM1, also known as p62)  and necroptosis that is dependent on receptor-interacting protein kinases 1 and 3 (RIPK1/RIPK3) .
SQSTM1 splice site mutation in distal myopathy with rimmed vacuoles.
We identified four novel methylation loci in PLA2G2C, SQSTM1, SLC4A4, and IGH that were strongly associated with arsenic exposure (p < 1 X [10.sup.-7]), as well as several suggestive associations in other gene regions.
LC3II also recognizes adaptor proteins like p62/ SQSTM1 which binds ubiquitinated proteins and transports them to the autophagosome.
Among these, one of the striking observations is the differential expression of numerous ALS-linked genes (i.e., ANG, DCTN1, SQSTM1, and TBK1) involved in autophagy, a highly conserved and tightly regulated cellular self-degradative process whose alteration leads to an impaired clearance of toxic protein aggregates and/or of damaged mitochondria that represent some of the best characterized hallmarks of both SALS and FALS .
Interestingly, both NAFLD and AFL are histologically characterized by impaired autophagy associated with prominent SQSTM1 protein accumulation in the form of cytoplasmic inclusions, histologically known as Mallory bodies [74, 84].
Many proteins are involved in autophagy, including autophagy-related proteins (ATGs), mammalian target of rapamycin (mTOR), the serine/threonine kinase (ULK1), FIP-200, p62 (SQSTM1), and microtubule-associated protein light chain 3 (LC3) .
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