Results 61 to 70 of about 9,804 (231)

Plakoglobin Suppresses Epithelial Proliferation and Hair Growth in Vivo [PDF]

The Journal of Cell Biology, 2000
Plakoglobin regulates cell adhesion by providing a modulatable connection between both classical and desmosomal cadherins and their respective cytoskeletal linker proteins. Both plakoglobin and the related protein β-catenin are posttranscriptionally upregulated in response to Wnt-1 in cultured cells.
Charpentier, Emmanuelle, Lavker, Robert M., Cowin, Pamela, Acquista, Elizabeth   +3 more
openaire   +3 more sources

Expression of desmosomal proteins and their implications during enamel organ morphogenesis

Indian Journal of Dental Sciences, 2018
Background/Objective: The present article is between the fewest that describe the expression of desmosomal proteins in human tooth organ and to implicate desmosome and its components in tooth morphogenesis.
Hadi BILAL
doaj   +1 more source

Molecular alterations that drive breast cancer metastasis to bone. [PDF]

, 2015
Epithelial cancers including breast and prostate commonly progress to form incurable bone metastases. For this to occur, cancer cells must adapt their phenotype and behaviour to enable detachment from the primary tumour, invasion into the vasculature ...
Friedrich RE, Karakosta A, Kim MS, Liang Z, Mackinder MA, Pé, Paget S, Powell GJ, Singh RK, Taichman RS, Takayama S, van der Pluijm G, Vesuna F   +12 more
core   +1 more source

Erythrokeratodermia‐Cardiomyopathy Syndrome: Expanding the DSP Mutational Spectrum Beyond Proline Substitutions

Pediatric Dermatology, EarlyView.
ABSTRACT Erythrokeratodermia cardiomyopathy (EKC) syndrome is a rare autosomal dominant disorder characterized by generalized erythrokeratoderma and progressive dilated cardiomyopathy, caused by pathogenic variants in the SR6 domain of desmoplakin (DSP).
Sepideh Hamzehlou, Ryland D. Mortlock, Caroline Echeandia‐Francis, Jing Zhou, Chao Xing, Nnenna G. Agim, Keith A. Choate, Donald A. Glass II   +7 more
wiley   +1 more source

Naxos Disease [PDF]

, 2005
Since 1995, according to the World Health Organisation’s classification of cardiomyopathies, Naxos disease has been considered as the recessive form of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).1 It is a stereotype association of
Protonotarios, Nikos, Tsatsopoulou, Adalena   +1 more
core   +2 more sources

Mitochondrial Adaptation to Mechanical Stress in Cardiac Ageing and Disease

Advanced Science, Volume 13, Issue 4, 19 January 2026.
Mechanical forces shape the heart's energy factories. This review explores how mitochondria in cardiac cells sense and respond to biomechanical stress, altering their structure, positioning, and metabolism. By linking mechanical cues to mitochondrial adaptation, the article highlights pathways driving heart disease and points to new strategies for ...
Aishwarya Prakash, Thomas Iskratsch
wiley   +1 more source

Functional Effects of the TMEM43 Ser358Leu Mutation in the Pathogenesis of Arrhythmogenic Right Ventricular Cardiomyopathy [PDF]

, 2012
Background: The Ser358Leu mutation in TMEM43, encoding an inner nuclear membrane protein, has been implicated in arrhythmogenic right ventricular cardiomyopathy (ARVC). The pathogenetic mechanisms of this mutation are poorly understood.
Ahmad, Ferhaan, McDonough, Barbara Anne, Rajkumar, Revathi, Seidman, Christine Edry, Sembrat, John C   +4 more
core   +5 more sources

Hypothesis: Ephrin–Eph Signaling Pathways Provide Novel Targets for Accelerated Re‐Epithelialization of Cutaneous Wounds

BioEssays, Volume 48, Issue 1, January 2026.
In distal limb wounds on the horse, the proliferative phase of repair often produces excessive granulation tissue that delays healing by impeding keratinocyte migration from wound margins. This essay examines the basis for the hypothesis that ephrin–Eph signaling pathways that stimulate keratinocyte migration provide novel targets for re‐establishing ...
Rodolfo D. Vicetti Miguel, Mohan Liu, Gabriel J. Campion, Thomas L. Cherpes   +3 more
wiley   +1 more source

Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations [PDF]

, 2016
Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disease caused by defective prelamin A processing, leading to nuclear lamina alterations, severe cardiovascular pathology, and premature death.
Benítez Iglesias, Raúl, Caballero, Ricardo, Cabello, Nuria, Calvo, Conrado J., González Gómez, Cristina, Gordon, Leslie B., Guadix, Juan A., Gúzman Martínez, Gabriela, Herraiz Martínez, Adela, Jiménez Borreguero, Luís J., Llach, Anna, López Otín, Carlos, Osorio, Fernando G., Riveras Torres, Jose, Vallmitjana Lees, Alexander   +14 more
core   +2 more sources

Decreased RYR2 Cluster Size and Abnormal SR Ca2+ Release Contribute to Arrhythmogenesis in TMEM43‐Related ARVC

Advanced Science, Volume 12, Issue 45, December 4, 2025.
The TMEM43 ‐ P386S mutation causes arrhythmogenic right ventricular cardiomyopathy (ARVC) by mislocalizing itself from nuclear envelope (NE) to cytoplasm, disrupting lamin B2 (a novel TMEM43 interactor) localization, NE integrity and chromatin accessibility, causing hyper ‐ phosphorylation and reduced expression/clustering of ryanodine receptor type 2 (
Jiaxi Shen, Xiaochen Wang, Hangping Fan, Yaxun Sun, Tingyu Gong, Hangyuan Qiu, Jue Wang, Ziwei Pan, Yanna Dang, Hongkun Wang, Danni Zhou, Tianyi Zhu, Hao Wang, Xianzhen Chen, Lizhen Xu, Jun Su, Fan Yang, Yiquan Tang, Xuguang Li, Bing Yang, Lenan Zhuang, Wei Wang, Chenyang Jiang, Ping Liang   +23 more
wiley   +1 more source