NM23-H1 Tumor Suppressor Physically Interacts with Serine-Threonine Kinase Receptor-associated Protein, a Transforming Growth Factor-β (TGF-β) Receptor-interacting Protein, and Negatively Regulates TGF-β Signaling [PDF]
, 2007 Hyun‐A Seong +2 more
openalex +1 more source
Covalent Reprogramming of Kinase Binders to Modulate Protein Abundance
Advanced Science, EarlyView.Electrophilic remodeling of a broad‐spectrum kinase binder reveals how subtle chemical changes reprogram protein fate. An acrylamide analog of a multi‐kinase binder selectively stabilizes Aurora kinase A (AURKA) by suppressing its ubiquitination, while a short‐linker variant converts this stabilizer into a degrader.
Chen Mozes +4 more
wiley +1 more source
Mechanosensitive Piezo1/Osteocalcin/Irisin Axis Protects Against Disuse‐Induced Muscle Atrophy
Advanced Science, EarlyView.Mechanical unloading suppresses bone Piezo1 expression, which reduces circulating undercarboxylated osteocalcin (unOCN). unOCN reduction subsequently exacerbates IMM‐induced Fndc5/Irisin decrease and drives severe muscle atrophy. Bone Piezo1 activation or exogenous osteocalcin/Irisin ameliorate muscle atrophy, while muscle‐specific Gprc6a or Fndc5 ...
Zhaolu Wang +5 more
wiley +1 more source
Activation of type II calcium/calmodulin-dependent protein kinase by Ca^(2+)/calmodulin is inhibited by autophosphorylation of threonine within the calmodulin-binding domain [PDF]
, 1990 It is now well established that autophosphorylation of a threonine residue located next to each calmodulin-binding domain in the subunits of type II Ca^(2+)/calmodulin-dependent protein kinase causes the kinase to remain active, although at a reduced ...
Kennedy, Mary B. +2 more
core
CK2α Deficiency Drives Myocardial Fibrosis via Desmin‐Induced Mitochondrial Dysfunction
Advanced Science, EarlyView.CK2α preserves mitochondrial homeostasis by phosphorylating Desmin to recruit Cryab, ensuring proper filament assembly. CK2α deficiency disrupts this interaction, causing mitochondrial dysfunction, metabolic shifts, bioenergetic failure, and oxidative stress—ultimately establishing a pro‐fibrotic environment that drives cardiac fibrosis.
Canjie Ma +12 more
wiley +1 more source
Mediators of Inflammation, 2014 Inflammation is a natural host defensive process that is largely regulated by macrophages during the innate immune response. Mitogen-activated protein kinases (MAPKs) are proline-directed serine and threonine protein kinases that regulate many ...
Yanyan Yang +7 more
doaj +1 more source
Therapy for Myhre Syndrome: Goals, Misconceptions, and Current Agents
American Journal of Medical Genetics Part C: Seminars in Medical Genetics, EarlyView.ABSTRACT Myhre Syndrome (MYHRS, MIM #139210) is a rare, multisystem connective tissue disorder caused by recurrent heterozygous gain‐of‐function pathogenic variants in the SMAD4 gene, a key player in TGF‐β signaling and a regulator of extracellular matrix homeostasis.
Alessandro De Falco +2 more
wiley +1 more source
A comprehensive proteome and phosphoproteome atlas across nine organs of the Chinese hamster
Animal Models and Experimental Medicine, EarlyView.This study presents the first comprehensive proteome and phosphoproteome atlas of the Chinese hamster across nine organs (heart, liver, lung, kidney, spleen, cerebral cortex, skeletal muscle, stomach, and testis or ovary). A total of 14 219 proteins were identified in the proteome, with 11 828 phosphorylated proteins and 47 122 phosphorylation sites ...
Luyao Zhang +15 more
wiley +1 more source
Annals of Neurology, EarlyView.Objective The extent of neuronal loss in Parkinson's disease (PD) and the pathogenic processes underlying neuronal dysfunction and loss remain poorly understood. Here, we analyzed the expression of key molecules representing different cell death signaling pathways and their association with Lewy pathology, dopaminergic (DA) neuron loss and stage of PD ...
Yue Jing Heng +3 more
wiley +1 more source