Results 151 to 160 of about 8,444 (178)

The seminal plasma proteome dataset of the giant panda. [PDF]

Data Brief
Zhou S, Wang T, Chen J, Li F, Wang S, Hu X, Zhang M, Hou R, Liu Y, Cai K.   +9 more
europepmc   +1 more source

Hyperoside protects against poly-GR-mediated neurodegeneration via regulation of mitochondrial fission and oxidative stress in C9orf72-associated ALS. [PDF]

Chin Med
Hsieh WC, Lin CY, Wu HC, Weng EF, Wang SM.   +4 more
europepmc   +1 more source

Genetic epidemiology of C9orf72 repeat expansion associated amyotrophic lateral sclerosis in Hungary. [PDF]

Mol Med
Nagy ZF, Géresi A, Grosz Z, Trombitás B, Pál M, Nagy D, Salamon A, Balicza P, Dézsi L, Klivényi P, Széll M, Molnár MJ.   +11 more
europepmc   +1 more source

Designing polymer-peptide conjugates to target dipeptide repeat aggregates implicated in amyotrophic lateral sclerosis.

J Mater Chem B
Gray VP, Cui Z, Klepsig M, Letteri RA.
europepmc   +1 more source

Repeated repeat problems: Combinatorial effect of C9orf72-derived dipeptide repeat proteins

International Journal of Biological Macromolecules, 2019
A microsatellite expansion mutation in C9orf72 is the most common genetic cause of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD). The expansion mutation leads to C9orf72 loss of function, RNA foci formation, and generation of five species of non-AUG RAN translated dipeptide repeat proteins (DPRs), such as poly(GA), poly(GP ...
April L Darling, Leonid Breydo, Dali Zheng   +2 more
exaly   +5 more sources

The C9orf72 GGGGCC Repeat Is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS

Science, 2013
Abstract: Expansion of a GGGGCC hexanucleotide repeat upstream of the C9orf72 coding region is the most common cause of familial frontotemporal lobar degeneration and amyotrophic lateral sclerosis (FTLD/ALS), but the pathomechanisms involved are unknown.
Kohji Mori, Thomas Arzberger, Stephanie May   +2 more
exaly   +3 more sources

Chimeric Peptide Species Contribute to Divergent Dipeptide Repeat Pathology in c9ALS/FTD and SCA36

Neuron, 2020
GGGGCC hexanucleotide repeat expansions (HREs) in C9orf72 cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and lead to the production of aggregating dipeptide repeat proteins (DPRs) via repeat associated non-AUG (RAN ...
Zachary T Mceachin, Tania F Gendron, Nisha Raj   +2 more
exaly   +3 more sources

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Reduced hn RNPA 3 increases C9orf72 repeat RNA levels and dipeptide‐repeat protein deposition

EMBO Reports, 2016
Intronic hexanucleotide (G4C2) repeat expansions in C9orf72 are genetically associated with frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). The repeat RNA accumulates within RNA foci but is also translated into disease characterizing dipeptide repeat proteins (DPR).
Kohji Mori, Thomas Arzberger, Qihui Zhou   +2 more
exaly   +2 more sources

Designed leucine‐rich repeat proteins bind two muramyl dipeptide ligands

Protein Science, 2021
AbstractDesigned protein receptors hold diagnostic and therapeutic promise. We now report the design of five consensus leucine‐rich repeat proteins (CLRR4–8) based on the LRR domain of nucleotide‐binding oligomerization domain (NOD)‐like receptors involved in the innate immune system.
Christina S. Kim, Anne M. Brown, Tijana Z. Grove, Felicia A. Etzkorn   +3 more
openaire   +2 more sources