Results 61 to 70 of about 7,866 (244)

Steric regulation of tandem calponin homology domain actin-binding affinity. [PDF]

, 2019
Tandem calponin homology (CH1-CH2) domains are common actin-binding domains in proteins that interact with and organize the actin cytoskeleton. Despite regions of high sequence similarity, CH1-CH2 domains can have remarkably different actin-binding ...
Bausch, Andreas, Belardi, Brian, Fletcher, Daniel A, Harris, Andrew R, Jreij, Pamela, Shams, Hengameh, Wei, Kathy   +6 more
core   +1 more source

Dystroglycan versatility in cell adhesion: a tale of multiple motifs [PDF]

, 2010
Dystroglycan is a ubiquitously expressed heterodimeric adhesion receptor. The extracellular a-subunit makes connections with a number of laminin G domain ligands including laminins, agrin and perlecan in the extracellular matrix and the transmembrane b-
A Ivetic, A Sgambato, A Waite, AJ Baines, AM Belkin, AS Yatsenko, AS Yatsenko, Avd Flier, B Casar, B Casar, B Yang, C Anderson, C Anderson, C Batchelor, C Berthier, C Losasso, C Moore, C Vanni, Chris J Moore, CL Batchelor, CL Batchelor, CM Gould, ED Apel, F Sotgia, F Sotgia, F Sotgia, FM Pavalko, GA Rezniczek, GC Dobbins, HJ Spence, HJ Spence, HJ Spence, J Iida, J Kahl, JCR Jones, JL Ilsley, JL Ilsley, JS Poulton, JW Legg, K Iida, K Russo, K Sumita, K Takahashi, K Takahashi, KJ Langenbach, KR Legate, L Fuentes-Mera, L Heiska, M Bartoli, M Bozzi, M Cavaldesi, M Durbeej, M Durbeej, M Ferletta, M Gautam, M James, M Schneider, M Villarreal-Silva, M Weir, ML Oppizzi, NR Smalheiser, NR Smalheiser, O Ibraghimov-Beskrovnaya, O Thompson, O Thompson, R González-Ramírez, RA Williamson, RM Grady, RO Hynes, S Cross, S Yonemura, SA Oak, SH Gee, SJ Winder, SJ Winder, Steve J Winder, T Haenggi, T Muranen, T Rando, V Mirouse, VJ Fincham, W-M Deng, X Yongmin, Y Lai, Y-J Chen, YW Zhou   +85 more
core   +3 more sources

Sticky utrophin messages

The Journal of Cell Biology, 2001
![Graphic][1] Utrophin mRNAs bind to actin. On [page 1173][2], Gramolini et al. report that utrophin mRNA is immobilized by binding to an actin-dependent structure. Manipulation of this system may be important for the therapy of Duchenne muscular dystrophy (DMD).
openaire   +2 more sources

Proteomic Profiling of Myofiber Repair Annexins and Their Role in Duchenne Muscular Dystrophy

PROTEOMICS, EarlyView.
ABSTRACT Myofiber regeneration and membrane repair play crucial roles in maintaining the continuous physiological functioning of the neuromuscular system. A swift and efficient repair mechanism enables the rapid restoration of sarcolemmal integrity following cellular impairment in damaged skeletal muscles.
Paul Dowling, Dounia Bouragba, Elisa Negroni, Capucine Trollet, Margit Zweyer, Dieter Swandulla, Kay Ohlendieck   +6 more
wiley   +1 more source

Evidence for ACTN3 as a genetic modifier of Duchenne muscular dystrophy [PDF]

, 2017
Duchenne muscular dystrophy (DMD) is characterized by muscle degeneration and progressive weakness. There is considerable inter-patient variability in disease onset and progression, which can confound the results of clinical trials.
, Bello, Luca, Gordish-Dressman, Heather, Head, Stewart I., Hoffman, Eric P., Hogarth, Marshall W., Houweling, Peter J., North, Kathryn N., Pegoraro, Elena, Thomas, Kristen C.   +9 more
core   +2 more sources

Current Trends in Duchenne Muscular Dystrophy Research and Therapy: 3D Cardiac Modelling

Journal of Cachexia, Sarcopenia and Muscle, Volume 17, Issue 1, February 2026.
ABSTRACT Duchenne muscular dystrophy (DMD), caused by dystrophin deficiency, presents a multifaceted challenge that affects both skeletal muscle function and cardiomyocyte homeostasis, causing progressive degeneration and life‐threatening cardiac complications by adolescence.
Marta Przymuszała, Marta Białobrzeska, Józef Dulak, Urszula Florczyk‐Soluch   +3 more
wiley   +1 more source

The impact of Hnrnpl deficiency on transcriptional patterns of developing muscle cells

FEBS Open Bio, Volume 16, Issue 1, Page 178-198, January 2026.
We performed nanopore whole‐transcriptome sequencing comparing RNA from Hnrnpl‐knockdown versus control C2C12 myoblasts to investigate the contributions of Hnrnpl to muscle development. Our results indicate that Hnrnpl regulates the expression of genes involved with Notch signaling and skeletal muscle, particularly splicing patterns of specific muscle ...
Hannah R. Littel, Mekala Gunasekaran, Audrey L. Daugherty, Natalya M. Wells, Johnnie Turner, Christine C. Bruels, Christina A. Pacak, Isabelle Draper, Peter B. Kang   +8 more
wiley   +1 more source

Obestatin Treatment Counteracts Muscle Wasting by Reactivation of Autophagy in Duchenne Muscular Dystrophy

MedComm, Volume 7, Issue 1, January 2026.
Obestatin signaling reactivates autophagy by NEDD4‐L activation under DMD conditions. Tyrosine switch on NEDD4‐L activates autoubiquitination that serves as a scaffold to recruit USP10 to form a deubiquitination complex, which stabilizes VPS34 to promote autophagy by activation of the Beclin1 complex. In parallel, NEDD4‐L favors AMPK exposure to CaMKKß
Icía Santos‐Zas, Silvia Costas‐Abalde, Andrea C. Lodeiro, Fátima Fernández‐Barreiro, Tania Cid‐Díaz, Saúl Leal‐López, Jessica González‐Sánchez, Mar García‐Lamela, Lucía Debasa‐Corral, Carlos S. Mosteiro, Kamel Mamchaoui, Vincent Mouly, Xesús Casabiell, Rosalía Gallego, José Luis Relova, Yolanda Pazos, Jesus P. Camiña   +16 more
wiley   +1 more source

Muscle-Specific SIRT1 Gain-of-Function Increases Slow-Twitch Fibers and Ameliorates Pathophysiology in a Mouse Model of Duchenne Muscular Dystrophy [PDF]

, 2013
SIRT1 is a metabolic sensor and regulator in various mammalian tissues and functions to counteract metabolic and age-related diseases. Here we generated and analyzed mice that express SIRT1 at high levels specifically in skeletal muscle.
Chalkiadaki, Angeliki, Guarente, Leonard Pershing, Igarashi, Masaki, Knezevic, Jovana, Nasamu, Armiyaw Sebastian   +4 more
core   +3 more sources

Repression-free utrophin-A 5'UTR variants.

Molecular biology research communications, 2019
Mutation in the dystrophin gene results Duchenne Muscular Dystrophy (DMD), an X-linked fatal neuromuscular disorder. Dystrophin deficiency can be compensated by upregulation of utrophin, an autosomal homologue of dystrophin. But the expression of utrophin in adults is restricted to myotendinous and neuromuscular junctions.
Malik, Debasish, Basu, Utpal
openaire   +2 more sources