Results 51 to 60 of about 786 (183)

Generation and Characterization of Twist1 Acetyl‐Mimic and Acetyl‐Deficient Mouse Models

open access: yesgenesis, Volume 64, Issue 3, June 2026.
ABSTRACT TWIST1 encodes a highly conserved basic helix–loop–helix transcription factor essential for embryonic development from Drosophila to humans. TWIST1 activity is regulated by post‐translational modifications, including phosphorylation during development and cancer metastasis. Recent cancer studies identified acetylation of lysines K73 and K76 as
Mary Elmeniawi   +6 more
wiley   +1 more source

Fibrodysplasia Ossificans Progressive Two Forms of a Disease

open access: yesMajallah-i Dānishgāh-i ̒Ulūm-i Pizishkī-i Bābul, 2010
BACKGROUND AND OBJECTIVE: Fibrodysplasia ossificans progressive (FOP) or myositis ossificans progressiva is a rare hereditary connective tissue disorder.
Y Aghighi,   +3 more
doaj  

Genetic Bone Diseases: A Scoping Review of Pathology, Symptoms, Diagnosis, Treatment, and New Horizons

open access: yesAdvanced Genetics, Volume 7, Issue 2, June 2026.
This review highlights six genetic diseases of the bone, aiming to provide clinicians and researchers with updated information on their diagnosis and treatment. It also includes an assessment of common clinical and radiographic findings, along with pathophysiology related to diseases.
Colin Jones, Ambalangodage C. Jayasuriya
wiley   +1 more source

Engineered Nestin+ TSPC‐Derived Exosomes Promote Tendon Repair Via Metabolic Reprogramming

open access: yesJournal of Extracellular Vesicles, Volume 15, Issue 6, June 2026.
Engineered Nestin+ TSPC‐derived exosomes promote tendon repair by reprogramming tenocyte metabolism via the pantothenate‐CoA‐mitochondria axis. They enhance mitochondrial function, reduce senescence and oxidative stress, restoring tendon structure and function in injured and aged models.
Linxiang Cheng   +8 more
wiley   +1 more source

A Network‐Based Approach to Understanding Key Signaling Pathways in Intervertebral Disc Biology

open access: yesJOR SPINE, Volume 9, Issue 2, June 2026.
A literature‐based signaling network capturing the most relevant pathways in human nucleus pulposus cells was first constructed from curated biological evidence. The network was then translated into a system of ordinary differential equations to derive steady‐state solutions and define median baseline activity levels.
Sofia Tseranidou   +11 more
wiley   +1 more source

Long-term follow-up of a pseudohypoparathyroidism type 1a patient with missense mutation (pro115ser) in exon 5

open access: yes, 2010
Pseudohypoparathyroidism (PHP) refers to end-organ resistance that primarily impairs the renal actions of parathyroid hormone (PTH). The patients with PHP type Ia (PHP-Ia), one of the 4 types of PHP, show resistance to other peptide hormones as well as ...
Şıklar, Zeynep   +5 more
core   +1 more source

Deletion of a Pax1 Sex‐Associated Genomic Region Associated With Adolescent Idiopathic Scoliosis Leads to Disc Degeneration, Instability, and Vertebral Rotation in Mice

open access: yesJOR SPINE, Volume 9, Issue 2, June 2026.
Overview of the effects of Pax1‐SAR deletion on gene expression, IVD degeneration, and resultant scoliotic‐like curvature between sexes. Proposed mechanism of sex‐dependent changes in gene expression in females (right) and males (left), resulting in sex‐dependent disc degeneration and scoliotic phenotypes.
Edward C. Moody   +4 more
wiley   +1 more source

DE L'ORIGINE DES OSSIFICATIONS ECTOPIQUES DANS LE SYSTEME NERVEUX CENTRAL

open access: yes, 1973
The influences affecting the development of an ectopic ossification process are reviewed. It is concluded that foci of ossifications found in the central nervous system are a particular instance of a more general phenomenon, always beginning with some ...
Danis, André
core  

Diagnosis and approach of pseudohypoparathyroidism type 1A and related disorders during long term follow-up: a case report

open access: yes
20.500.12530/87873Objectives: Pseudohypoparathyroidism type 1A (PHP1A) encompasses the association of resistance to multiple hormones, features of Albright hereditary osteodystrophy and decreased Gs alpha activity.
Raspeno, Monica Exposito   +6 more
core   +1 more source

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