Results 11 to 20 of about 57,370,564 (168)

p62/Sequestosome-1 Is Indispensable for Maturation and Stabilization of Mallory-Denk Bodies.

PLoS ONE, 2016
Mallory-Denk bodies (MDBs) are hepatocytic protein aggregates found in steatohepatitis and several other chronic liver diseases as well as hepatocellular carcinoma. MDBs are mainly composed of phosphorylated keratins and stress protein p62/Sequestosome-1
Pooja Lahiri, Volker Schmidt, Claudia Smole, Iris Kufferath, Helmut Denk, Pavel Strnad, Thomas Rülicke, Leopold F Fröhlich, Kurt Zatloukal   +8 more
doaj   +3 more sources

TAK1 converts Sequestosome 1/p62 from an autophagy receptor to a signaling platform [PDF]

EMBO Reports, 2019
The protein p62/Sequestosome 1 (p62) has been described as a selective autophagy receptor and independently as a platform for pro‐inflammatory and other intracellular signaling.
Stephanie R Kehl, Brandy-Lee Soos, B. Saha, Seong Won Choi, Anthony W. Herren, T. Johansen, M. Mandell   +6 more
semanticscholar   +2 more sources

Alterations of the 70 kDa heat shock protein (HSP70) and sequestosome-1 (p62) in women with breast cancer

Scientific Reports, 2021
Peripheral blood mononuclear cells (PBMCs) respond to altered physiological conditions to alleviate the threat. Production of the 70 kDa heat shock protein (HSP70) is up-regulated to protect proteins from degradation.
Theofano Orfanelli, Spyridon Giannopoulos, Eleni Zografos, Aikaterini Athanasiou, Ann Marie Bongiovanni, Georgios Doulaveris, Tracy-Ann Moo, Dayle LaPolla, Chris N. Bakoyiannis, Georgios E. Theodoropoulos, Georgios C. Zografos, Eleni Andreopoulou, Steven S. Witkin   +12 more
doaj   +2 more sources

The converging roles of sequestosome-1/p62 in the molecular pathways of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD)

Neurobiology of Disease, 2022
Investigations into the pathogenetic mechanisms underlying amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) have provided significant insight into the disease.
Jennilee M. Davidson, Roger S. Chung, Albert Lee   +2 more
doaj   +2 more sources

Immunohistochemical Profile of p62/SQSTM1/Sequestosome-1 in Human Low- and High-Grade Intracranial Meningiomas

Analytical Cellular Pathology
Among autophagic-related proteins, p62/SQSTM1/Sequestosome-1 represents a relevant actor in cellular proliferation and neoplastic growth. Although, recently, p62 expression has been analyzed in different neurodegenerative and glial neoplastic diseases ...
Antonio Ieni, Cristina Pizzimenti, Vincenzo Fiorentino, Mariausilia Franchina, Antonino Germanò, Giovanni Raffa, Maurizio Martini, Guido Fadda, Giovanni Tuccari   +8 more
doaj   +2 more sources

A proximity-dependent biotinylation (BioID) approach flags the p62/sequestosome-1 protein as a caspase-1 substrate

Journal of Biological Chemistry, 2018
The inflammasome is a major component of the innate immune system, and its main function is to activate caspase-1, a cysteine protease that promotes inflammation by inducing interleukin-1β (IL-1β) maturation and release into the extracellular milieu.
Y. Jamilloux, B. Lagrange, A. Di Micco, E. Bourdonnay, Angélina Provost, Rémy Tallant, T. Henry, F. Martinon   +7 more
semanticscholar   +2 more sources

Sequestosome-1/p62 Mediates TLR4-Induced Inflammatory Program in Dendritic Cells Under Normoxic and Hypoxic Conditions

Cellular and Molecular Life Sciences
Sequestosome-1/p62, a multifunctional adaptor protein, plays a critical role in NFκB signaling. In response to Toll-like receptor 4 (TLR4) activation, p62 facilitates NFκB activation via its interaction with RIP1, a process dependent on the p62 ZZ-domain.
Federica Coppola, Sara Monaci, Alessandro Falsini, Irene Filippi, Carlo Aldinucci, Fabio Carraro, Antonella Naldini   +6 more
doaj   +2 more sources

p62/SQSTM1/Sequestosome-1 is an N-recognin of the N-end rule pathway which modulates autophagosome biogenesis

Nature Communications, 2017
Soluble misfolded proteins that fail to be degraded by the ubiquitin proteasome system (UPS) are redirected to autophagy via specific adaptors, such as p62.
Hyunjoo Cha-Molstad, Ji Eun Yu, Zhiwei Feng, Su Hyun Lee, Jung Gi Kim, Peng Yang, Bitnara Han, Ki Woon Sung, Young Dong Yoo, Joonsung Hwang, Terry McGuire, Sang Mi Shim, Hyun Dong Song, Srinivasrao Ganipisetti, Nuozhou Wang, Jun Min Jang, Min Jae Lee, Seung Jun Kim, Kyung Ho Lee, Jin Tae Hong, Aaron Ciechanover, Inhee Mook-Jung, Kwang Pyo Kim, Xiang-Qun Xie, Yong Tae Kwon, Bo Yeon Kim   +25 more
doaj   +2 more sources

Sequestering sequestosome 1 via S-acylation in autophagy, Huntington disease, and beyond

Autophagy Reports
Protein mislocalization and aggregation are hallmark features in neurodegeneration. As proteins mislocalize, proteostasis deficiency and protein aggregation typically follow.
Y Alshehabi, F Abrar, D.D.O Martin
doaj   +2 more sources

Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice

Frontiers in Neuroscience, 2017
Neuronal degeneration following traumatic brain injury (TBI) leads to intracellular accumulation of dysfunctional proteins and organelles. Autophagy may serve to facilitate degradation to overcome protein debris load and therefore be an important pro ...
Anne Sebastiani, Christina Gölz, Philipp G. Sebastiani, Wiesia Bobkiewicz, Christian Behl, Thomas Mittmann, Serge C. Thal, Kristin Engelhard   +7 more
doaj   +2 more sources