Results 91 to 100 of about 28,592 (236)

Alteration of Sarcoplasmic Reticulum Ca2+ Release in Skeletal Muscle from Calpain 3-Deficient Mice

open access: yesInternational Journal of Cell Biology, 2009
Mutations of Ca2+-activated proteases (calpains) cause muscular dystrophies. Nevertheless, the specific role of calpains in Ca2+ signalling during the onset of dystrophies remains unclear.
Govindan Dayanithi   +11 more
doaj   +1 more source

Comparison of Calpain and Caspase Activities in the Adult Rat Brain after Transient Forebrain Ischemia

open access: yesNeurobiology of Disease, 2002
The role of calpain and caspase family proteases in postischemic neuronal death remains controversial. This study compared the timing, location, and relative activity of calpains and caspases in the adult rat brain following 10 min of transient forebrain
Chen Zhang   +5 more
doaj   +1 more source

Calpain-3 is activated in KO lenses.

open access: yes, 2016
A. Immunostaining of 1-month old lens sections with anti-calpain Lp-85 antibody. KO lens show an increased expression of calpain compared to WT. Inset images a and b are enlarged areas of the equatorial region of WT and KO lens sections respectively ...
Robert A. Kesterson (342895)   +2 more
core   +1 more source

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

open access: yesPROTEOMICS, 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   +6 more
wiley   +1 more source

Broadening the View: Substance P and Its Metabolism in Pruritus‐Related Diseases

open access: yesThe Journal of Dermatology, EarlyView.
ABSTRACT Chronic pruritus is a debilitating symptom accompanying numerous inflammatory skin diseases and remains a major therapeutic challenge. Neurogenic inflammation plays a central role in its pathogenesis, with the tachykinin substance P acting as a key mediator at the interface of the nervous system, immune cells, and cutaneous tissues.
Thomas Walter, Bjoern B. Burckhardt
wiley   +1 more source

Minocycline in phenotypic models of Huntington's disease

open access: yesNeurobiology of Disease, 2005
Minocycline has been shown to be neuroprotective in various models of neurodegenerative diseases. However, its potential in Huntington's disease (HD) models characterized by calpain-dependent degeneration and inflammation has not been investigated. Here,
Kadiombo Bantubungi   +15 more
doaj   +1 more source

Red blood cell membrane proteome as a reporter of disease severity, transfusion impact and genetic background in transfusion‐dependent β‐thalassaemia

open access: yesBritish Journal of Haematology, EarlyView.
Summary Omics technologies have transformed research in haemoglobinopathies, yet the proteome of RBCs remains largely unexplored in transfusion‐dependent thalassaemia (TDT). In this proteomic analysis, Red blood cell (RBC) membranes from 48 adults with TDT were compared with healthy controls.
Konstantina Theocharaki   +8 more
wiley   +1 more source

Characterizing the Catalytic Action of μ-Calpain on Myofibrillar Protein Structure

open access: yes, 2006
Solving the problem of inconsistent meat tenderness is a top priority of the meat industry. This requires a greater understanding of the processes that affect meat tenderness and the adoption of such information by the meat industry. It is essential that
Fraser-Smith, Emma Louise
core  

KU80 suppresses endonuclease G activity to preserve genomic integrity

open access: yesThe FEBS Journal, EarlyView.
Under normal conditions, EndoG remains restricted to mitochondria and the genome remains intact. When KU80 is absent, EndoG translocates into the nucleus, where it promotes DNA fragmentation and genomic instability. Thus, this work highlights the importance of KU80 in tightly controlling EndoG localization to preserve genome stability.
Jargalan Batsaikhan   +8 more
wiley   +1 more source

Calpain 3 mRNA expression in mice after denervation and during muscle regeneration.

open access: yes, 2001
Lack of functional calpain 3 in humans is a cause of limb girdle muscular dystrophy, but the function(s) of calpain 3 remain(s) unknown. Special muscle conditions in which calpain 3 is downregulated could yield valuable clues to the understanding of its ...
Marchand, S.   +7 more
core   +2 more sources

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