scholarly journals The 1316T>C missenses mutation in MTHFR contributes to MTHFR deficiency by targeting MTHFR to proteasome degradation

Aging ◽  
2020 ◽  
Author(s):  
Xi Liu ◽  
Yu Li ◽  
Menghan Wang ◽  
Xiaojun Wang ◽  
Limin Zhang ◽  
...  
Keyword(s):  
Proteasome Degradation ◽  
Mthfr Deficiency

The Adaptor Molecule CIN85 Regulates Syk Tyrosine Kinase Level by Activating the Ubiquitin-Proteasome Degradation Pathway

2007 ◽  
Vol 179 (4) ◽  
pp. 2089-2096 ◽  
Author(s):  
Giovanna Peruzzi ◽  
Rosa Molfetta ◽  
Francesca Gasparrini ◽  
Laura Vian ◽  
Stefania Morrone ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Degradation Pathway ◽  
Proteasome Degradation ◽  
Adaptor Molecule ◽  
Ubiquitin Proteasome

scholarly journals Clinical pattern, mutations and in vitro residual activity in 33 patients with severe 5, 10 methylenetetrahydrofolate reductase (MTHFR) deficiency

2015 ◽  
Vol 39 (1) ◽  
pp. 115-124 ◽  
Author(s):  
Martina Huemer ◽  
Regina Mulder-Bleile ◽  
Patricie Burda ◽  
D. Sean Froese ◽  
Terttu Suormala ◽  
...  
Keyword(s):  
Methylenetetrahydrofolate Reductase ◽  
Residual Activity ◽  
Clinical Pattern ◽  
Mthfr Deficiency

scholarly journals Caspase-3-like activity and proteasome degradation in grapevine suspension cell cultures undergoing silver-induced programmed cell death

2019 ◽  
Vol 233 ◽  
pp. 42-51 ◽  
Author(s):  
Antonio Filippi ◽  
Marco Zancani ◽  
Elisa Petrussa ◽  
Enrico Braidot
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Cultures ◽  
Caspase 3 ◽  
Suspension Cell ◽  
Proteasome Degradation ◽  
Suspension Cell Cultures

E3 ubiquitin ligase CHIP interacts with C-type lectin-like receptor CLEC-2 and promotes its ubiquitin-proteasome degradation

2016 ◽  
Vol 28 (10) ◽  
pp. 1530-1536 ◽  
Author(s):  
Miaomiao Shao ◽  
Lili Li ◽  
Shushu Song ◽  
Weicheng Wu ◽  
Peike Peng ◽  
...  
Keyword(s):  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Proteasome Degradation ◽  
Ubiquitin Proteasome

scholarly journals Skp2 inhibits osteogenesis by promoting ubiquitin–proteasome degradation of Runx2

2016 ◽  
Vol 1863 (4) ◽  
pp. 510-519 ◽  
Author(s):  
Gatha Thacker ◽  
Yogesh Kumar ◽  
Mohd. Parvez Khan ◽  
Nidhi Shukla ◽  
Isha Kapoor ◽  
...  
Keyword(s):  
Proteasome Degradation ◽  
Ubiquitin Proteasome

422 URSODEOXYCHOLIC ACID MODULATES THE UBIQUITIN-PROTEASOME DEGRADATION PATHWAY OF P53

2008 ◽  
Vol 48 ◽  
pp. S162-S163
Author(s):  
J.D. Amaral ◽  
R.E. Castro ◽  
S. Sola ◽  
C.M.P. Rodrigues
Keyword(s):  
Ursodeoxycholic Acid ◽  
Degradation Pathway ◽  
Proteasome Degradation ◽  
Ubiquitin Proteasome

scholarly journals 4-Hydroxynonenal differentially regulates adiponectin gene expression and secretion via activating PPARγ and accelerating ubiquitin–proteasome degradation

2012 ◽  
Vol 349 (2) ◽  
pp. 222-231 ◽  
Author(s):  
Zhigang Wang ◽  
Xiaobing Dou ◽  
Dongfang Gu ◽  
Chen Shen ◽  
Tong Yao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adiponectin Gene ◽  
Proteasome Degradation ◽  
Ubiquitin Proteasome

Sex-dependent behavioral effects of Mthfr deficiency and neonatal GABA potentiation in mice

2011 ◽  
Vol 216 (2) ◽  
pp. 505-513 ◽  
Author(s):  
Tamar Levav-Rabkin ◽  
Elinor Blumkin ◽  
Dalia Galron ◽  
Hava M. Golan
Keyword(s):  
Behavioral Effects ◽  
Mthfr Deficiency

scholarly journals Evading the Proteasome: Absence of Lysine Residues Contributes to Pertussis Toxin Activity by Evasion of Proteasome Degradation

2007 ◽  
Vol 75 (6) ◽  
pp. 2946-2953 ◽  
Author(s):  
Zoë E. V. Worthington ◽  
Nicholas H. Carbonetti
Keyword(s):  
Pertussis Toxin ◽  
Intracellular Transport ◽  
Cellular Activity ◽  
Wild Type ◽  
Proteasome Degradation ◽  
Lysine Residues ◽  
Arginine Residues ◽  
A Subunit ◽  
Adp Ribosyltransferase

ABSTRACT Pertussis toxin (PT) is an important virulence factor produced by Bordetella pertussis. PT holotoxin comprises one enzymatically active A subunit (S1), associated with a pentamer of B subunits. PT is an ADP-ribosyltransferase that modifies several mammalian heterotrimeric G proteins. Some bacterial toxins are believed to undergo retrograde intracellular transport through the Golgi apparatus to the endoplasmic reticulum (ER). The ER-associated degradation (ERAD) pathway involves the removal of misfolded proteins from the ER and degradation upon their return to the cytosol; this pathway may be exploited by PT and other toxins. In the cytosol, ERAD substrates are ubiquitinated at lysine residues, targeting them to the proteasome for degradation. We hypothesize that S1 avoids ubiquitination and proteasome degradation due to its lack of lysine residues. We predicted that the addition of lysine residues would reduce PT toxicity by allowing ubiquitination and degradation to occur. Variant forms of PT were engineered, replacing one, two, or three arginines with lysines in a variety of locations on S1. Several variants were identified with wild-type in vitro enzymatic activity but reduced cellular activity, consistent with our hypothesis. Significant recovery of the cellular activity of these variants was observed when CHO cells were pretreated with a proteasome inhibitor. We concluded that the replacement of arginine residues with lysine in the S1 subunit of PT renders the toxin subject to proteasomal degradation, suggesting that wild-type PT avoids proteasome degradation due to an absence of lysine residues.

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