Results 41 to 50 of about 17,002 (210)

Assays for protein retrotranslocation in ERAD [PDF]

open access: yes, 2019
Elimination of misfolded proteins by endoplasmic reticulum (ER)-associated protein degradation (ERAD) ensures that proteins proceeding through the secretory pathway are correctly folded and processed, which is critical to minimize ER stress.
Duttke, Sascha   +5 more
core   +1 more source

Stringent requirement for HRD1, SEL1L, and OS-9/XTP3-B for disposal of ERAD-LS substrates [PDF]

open access: yes, 2010
Sophisticated quality control mechanisms prolong retention of protein-folding intermediates in the endoplasmic reticulum (ER) until maturation while sorting out terminally misfolded polypeptides for ER-associated degradation (ERAD).
Bernasconi, Riccardo   +4 more
core   +4 more sources

Derlin-1 deficiency is embryonic lethal, Derlin-3 deficiency appears normal, and Herp deficiency is intolerant to glucose load and ischemia in mice. [PDF]

open access: yesPLoS ONE, 2012
Accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) causes a cellular condition called ER stress. To overcome ER stress, unfolded proteins are eliminated by an ER-associated degradation (ERAD) system.
Yuka Eura   +5 more
doaj   +1 more source

Eradication of Poliomyelitis

open access: yesAnnals of Internal Medicine, 1961
Excerpt Poliomyelitis, as well as many other infectious diseases, probably began their association with the human species long before human beings evolved in their present form.
openaire   +5 more sources

Defining human ERAD networks through an integrative mapping strategy [PDF]

open access: yes, 2011
Proteins that fail to correctly fold or assemble into oligomeric complexes in the endoplasmic reticulum (ER) are degraded by a ubiquitin-and proteasome-dependent process known as ER-associated degradation (ERAD).
Christianson, JC   +30 more
core   +1 more source

Ubiquitylation in ERAD: reversing to go forward? [PDF]

open access: yes, 2011
Proteins are co-translationally inserted into the endoplasmic reticulum (ER) where they undergo maturation. Homeostasis in the ER requires a highly sensitive and selective means of quality control.
Yien Che Tsai   +2 more
core   +1 more source

Huntingtin interacts with the cue domain of gp78 and inhibits gp78 binding to ubiquitin and p97/VCP. [PDF]

open access: yesPLoS ONE, 2010
Huntington's disease (HD) is caused by polyglutamine expansion in huntingtin (htt) protein, but the exact mechanism of HD pathogenesis remains uncertain.
Hui Yang   +5 more
doaj   +1 more source

Accurate and noninvasive prostate cancer detection using plasma‐derived extracellular vesicle RNA

open access: yesFEBS Open Bio, EarlyView.
Plasma extracellular vesicles were captured with WGA‐conjugated magnetic beads and profiled for RNA biomarkers. A three‐RNA panel (NM_024955, NR_047469, and NR_002564) distinguished prostate cancer from healthy controls and benign prostatic hyperplasia, supporting a simple, noninvasive approach to improve prostate cancer detection.
Hanping Wei, Haoran Wu, Wei Feng
wiley   +1 more source

Unraveling 4‐Phenylbutyrate's Therapeutic Role in SLC6A1 Disorders: Pharmacochaperoning Over HDAC Inhibition

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Variants in SLC6A1, encoding the GABA transporter 1 (GAT‐1), cause epilepsy, autism spectrum disorder, and developmental delay via loss of GABA uptake, impaired trafficking, and ER retention. We previously found that 4‐Phenylbutyrate (PBA), an FDA‐approved drug, restores GABA uptake and reduces seizures in SLC6A1‐related disorders ...
Melissa B. DeLeeuw   +5 more
wiley   +1 more source

Loss of E3 Ubiquitin Ligase RINES via CpG Methylation Relieves Suppression of STAT3 and MYC, Facilitating Multiple Tumorigeneses

open access: yesAdvanced Science, EarlyView.
Dysregulated protein modifications drive tumorigenesis. RINES, an E3 ubiquitin ligase, represses tumor cell proliferation and metastasis by facilitating RING domain‐dependent, ubiquitin–proteasome‐mediated degradation of STAT3 and MYC, which consequently restrains cancer stemness and oncogenic progression.
Lili Li   +8 more
wiley   +1 more source

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