Results 111 to 120 of about 40,761 (237)
Regulation of the actin–myosin interaction by titin [PDF]
Nicolas J. Niederländer +3 more
openalex +1 more source
This study advances top‐down individual ion mass spectrometry (I2MS) to profile intact phospho‐proteoforms of β‐ and α‐catenins (85–110 kDa) within cadherin–catenin complexes. By modulating actomyosin contractility, we reveal mechano‐sensitive phosphorylation patterns and propose that distinct catenin proteoforms may reflect adhesive states at cell ...
Che‐Fan Huang +4 more
wiley +2 more sources
Myosin VIIA gene: heterogeneity of the mutations responsible for Usher syndrome type IB [PDF]
G Lévy
openalex +1 more source
A six‐element viscoelastic model is presented for tissue‐engineered skeletal muscle, addressing the limitations of the conventional Hill's model. By introducing an active branch, the model accurately describes force responses in both elongation and isometric tests and successfully predicts the electrically induced displacement of a reverse‐action ...
Mizuki Nakamura +6 more
wiley +1 more source
Development of an efficient mice model of cancer‐associated cardiac cachexia
This work establishes a preclinical framework for targeting ubiquitin pathways to mitigate the morbidity of cancer‐related cardiopathy. Our integrated approach delineates a hierarchical progression from subcellular dysfunction to macroscopic cardiac deterioration. These findings mechanistically link tumor‐induced cachexia to cardiac dysfunction through
Shijie Xiong +9 more
wiley +1 more source
Biallelic Variants in the DARS2 Gene as a Novel Cause of Axonal Charcot–Marie–Tooth Disease
Objective Charcot–Marie–Tooth (CMT) disease is a heterogeneous group of genetic neuropathies, with >90 genes identified. Several aminoacyl‐tRNA synthetases have been linked to CMT. DARS2, encoding the mitochondrial aspartyl‐tRNA synthetase, has been typically associated with leukoencephalopathy with brainstem and spinal cord involvement and lactate ...
Berta Estévez‐Arias +23 more
wiley +1 more source
Objective Myotonic dystrophy type 1 (DM1) is a highly variable, multisystemic genetic disorder caused by a CTG repeat expansion in the 3′ untranslated region of DMPK. Toxicity is exerted by repeat‐containing DMPK transcripts that sequester muscleblind‐like (MBNL) proteins and lead to deleterious yet predictable changes in alternative splicing.
Samuel T. Carrell +3 more
wiley +1 more source
Figure S7 from Capping Protein Regulator and Myosin 1 Linker 3 Is Required for Tumor Metastasis
Huan Wang +6 more
openalex +1 more source

