Results 121 to 130 of about 870,777 (309)

A cell shrinkage artefact in growth plate chondrocytes with common fixative solutions: importance of fixative osmolarity for maintaining morphology [PDF]

open access: yesEuropean Cells & Materials, 2010
The remarkable increase in chondrocyte volume is a major determinant in the longitudinal growth of mammalian bones. To permit a detailed morphological study of hypertrophic chondrocytes using standard histological techniques, the preservation of normal ...
MY Loqman   +3 more
doaj  

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Leptin-deficient mice have altered three-dimensional growth plate histomorphometry

open access: yes, 2019
Background Leptin is an adipokine that regulates energy homeostasis and is also needed for normal bone growth and maintenance. Mutation in the lep gene, which characterizes the ob/ob mouse model, results in the development of obesity and type 2 diabetes ...
Monica Castro   +4 more
core   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

open access: yesMolecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober   +16 more
wiley   +1 more source

Analysis of risk factors for postoperative wound healing in children with bone cysts

open access: yesAnnals of Medicine
Background Bone cysts are common benign bone tumour-like lesions in children and adolescents. Postoperative wound healing complications significantly affect patient outcomes.
Muhan Yu, Yuxi Su
doaj   +1 more source

Finding novel vulnerabilities of hypomorphic BRCA1 alleles

open access: yesMolecular Oncology, EarlyView.
Synthetic lethality screens performed to identify novel vulnerabilities often model complete gene loss, thereby overlooking patient‐derived hypomorphic mutations. In this study, we have performed genome‐wide CRISPR screens on BRCA1 hypomorphic mutations, showing BRCA1I26A behaves like wild‐type, while BRCA1R1699Q mimics deficiency. Furthermore, we have
Anne Schreuder   +10 more
wiley   +1 more source

Transplantation of growth plate chondrocytes into growth plate defect in rabbit

open access: yes, 1999
We performed a procedure to transplant cultured growth plate chondrocyte embedded in type Ⅰ collagen gel into the defects of the proximal tibial physis in a 6-week-old rabbit.
이우석, 이진우
core  

Bortezomib significantly reduced growth plate height.

open access: yes, 2012
Representative pictures of mouse tibia growth plates on day 13 (A) and at termination of the experiment on day 56 (B). The thin black lines indicate the different zones within the growth plate; R (resting), P (proliferative) and H (hypertrophic).
Terhi J. Heino (114290)   +5 more
core   +1 more source

Impact of elevated sclerostin levels on bone resorption: unravelling structural changes and mineral metabolism disruption

open access: yesBone & Joint Research
Aims: The physiological function of sclerostin remains unknown. Sclerostin is synthesized by osteocytes and operates by inhibiting the Wnt/β-catenin pathway. Similarly, it is well established that low levels of sclerostin lead to enhanced bone formation
María Encarnacion Rodríguez-Ortiz   +12 more
doaj   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

open access: yesMolecular Oncology, EarlyView.
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir   +13 more
wiley   +1 more source

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