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HES factors regulate specific aspects of chondrogenesis and chondrocyte hypertrophy during cartilage development.
Timothy P Rutkowski et al.
Journal of cell science, 129(11), 2145-2155 (2016-05-11)
RBPjκ-dependent Notch signaling regulates multiple processes during cartilage development, including chondrogenesis, chondrocyte hypertrophy and cartilage matrix catabolism. Select members of the HES- and HEY-families of transcription factors are recognized Notch signaling targets that mediate specific aspects of Notch function during
Biglycan and fibromodulin have essential roles in regulating chondrogenesis and extracellular matrix turnover in temporomandibular joint osteoarthritis.
Embree, MC; Kilts, TM; Ono, M; Inkson, CA; Syed-Picard, F; Karsdal, MA; Oldberg, A; Bi, Y; Young, MF
The American Journal of Pathology null
Perineuronal Nets Suppress Plasticity of Excitatory Synapses on CA2 Pyramidal Neurons.
Kelly E Carstens et al.
The Journal of neuroscience : the of-ficial journal of the Society for Neuroscience, 36(23), 6312-6320 (2016-06-10)
Long-term potentiation of excitatory synapses on pyramidal neurons in the stratum radiatum rarely occurs in hippocampal area CA2. Here, we present evidence that perineuronal nets (PNNs), a specialized extracellular matrix typically localized around inhibitory neurons, also surround mouse CA2 pyramidal
Downregulation of HS6ST2 by miR-23b-3p enhances matrix degradation through p38 MAPK pathway in osteoarthritis.
Yuanxu Guo et al.
Cell death & disease, 9(6), 699-699 (2018-06-15)
Osteoarthritis (OA) is the most common form of arthritis involving major structural changes of peripheral joints and local or systemic inflammation and in lack of therapeutic approaches because of complexity of underlying molecular basis. Our previous work showed that HS6ST2
Aggrecan, link protein and tenascin-R are essential components of the perineuronal net to protect neurons against iron-induced oxidative stress.
Suttkus, A; Rohn, S; Weigel, S; Glockner, P; Arendt, T; Morawski, M
Cell Death & Disease null