Results 11 to 20 of about 21,246,065 (185)

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

EMBO Rep, 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. How these seemingly disparate functional roles of p62 are coordinated has not been resolved.
Kehl SR, Soos BA, Saha B, Choi SW, Herren AW, Johansen T, Mandell MA.   +6 more
europepmc   +7 more sources

p62/sequestosome-1 as a severity-reflecting plasma biomarker in Charcot–Marie–Tooth disease type 1A [PDF]

Scientific Reports
Autophagy is a self-degradation system for recycling to maintain homeostasis. p62/sequestosome-1 (p62) is an autophagy receptor that accumulates in neuroglia in neurodegenerative diseases.
Byeol-A Yoon, Young Hee Kim, Soo Hyun Nam, Hye-Jin Lee, Seong-il Oh, Namhee Kim, Kyeong-Hee Kim, Young Rae Jo, Jong Kuk Kim, Byung-Ok Choi, Hwan Tae Park   +10 more
doaj   +3 more sources

Enhanced neointimal hyperplasia and carotid artery remodelling in sequestosome 1 deficient mice [PDF]

Journal of Cellular and Molecular Medicine, 2010
AbstractDeficiency in the signal adaptor protein sequestosome 1 (SQSTM1/A170/p62) in mice is associated with mature‐onset obesity, accompanied by insulin and leptin resistance. We previously established that redox sensitive transcription factor Nrf2 up‐regulates SQSTM1 expression in response to atherogenic stimuli or laminar shear stress in vascular ...
Toru Yanagawa, Noriko Noguchi, Richard C M Siow   +2 more
exaly   +5 more sources

Deficiency of p62/Sequestosome 1 causes hyperphagia due to leptin resistance in the brain. [PDF]

J Neurosci, 2013
The cytoplasmic regulatory protein p62 (Sequestosome 1/A170) is known to modulate various receptor-mediated intracellular signaling pathways.p62deficiency was shown to result in mature-onset obesity in mice, but the mechanisms underlying this abnormality remained unclear.
Harada H, Warabi E, Matsuki T, Yanagawa T, Okada K, Uwayama J, Ikeda A, Nakaso K, Kirii K, Noguchi N, Bukawa H, Siow RC, Mann GE, Shoda J, Ishii T, Sakurai T.   +15 more
europepmc   +6 more sources

Sequestosome 1/p62 – More than just a scaffold [PDF]

FEBS Letters, 2006
The interaction of proteins with ubiquitin receptors is key to solving the mystery that surrounds the functional role ubiquitin chains play in directing traffic. The specificity of these interactions is largely mediated by UbL/UBA domains. Sequestosome 1/p62 is a protein that is gaining attention as it is intimately involved in cell signaling, receptor
Seibenhener, M. Lamar, Geetha, Thangiah, Wooten, Marie W.   +2 more
openaire   +3 more sources

The role of sequestosome 1/p62 protein in amyotrophic lateral sclerosis and frontotemporal dementia pathogenesis

Neural Regeneration Research, 2020
Amyotrophic lateral sclerosis and frontotemporal lobar degeneration are multifaceted diseases with genotypic, pathological and clinical overlap. One such overlap is the presence of SQSTM1/p62 mutations.
Adriana Delice Foster, Sarah Lyn Rea
doaj   +2 more sources

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

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

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

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

p62/sequestosome-1 knockout delays neurodegeneration induced by Drp1 loss. [PDF]

Neurochem Int, 2018
Purkinje neurons, one of the largest neurons in the brain, are critical for controlling body movements, and the dysfunction and degeneration of these cells cause ataxia. Purkinje neurons require a very efficient energy supply from mitochondria because of their large size and extensive dendritic arbors.
Yamada T, Adachi Y, Yanagawa T, Iijima M, Sesaki H.   +4 more
europepmc   +4 more sources

Tumorigenesis in tuberous sclerosis complex is autophagy and p62/sequestosome 1 (SQSTM1)-dependent [PDF]

Proceedings of the National Academy of Sciences, 2011
Tuberous sclerosis complex (TSC) is a tumor suppressor syndrome characterized by benign tumors in multiple organs, including the brain and kidney. TSC-associated tumors exhibit hyperactivation of mammalian target of rapamycin complex 1 (mTORC1), a direct inhibitor of autophagy. Autophagy can either promote or inhibit tumorigenesis,
Andrey, Parkhitko, Faina, Myachina, Tasha A, Morrison, Khadijah M, Hindi, Neil, Auricchio, Magdalena, Karbowniczek, J Julia, Wu, Toren, Finkel, David J, Kwiatkowski, Jane J, Yu, Elizabeth Petri, Henske   +10 more
openaire   +3 more sources