Relevant bibliographies by topics / Endoplasmic reticulum. Bones Cartilage

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Endoplasmic reticulum. Bones Cartilage'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Endoplasmic reticulum. Bones Cartilage"

1

Kambe, K., A. Yamamoto, T. Yoshimori, K. Hirayoshi, R. Ogawa, and Y. Tashiro. "Preferential localization of heat shock protein 47 in dilated endoplasmic reticulum of chicken chondrocytes." Journal of Histochemistry & Cytochemistry 42, no. 7 (1994): 833–41. http://dx.doi.org/10.1177/42.7.8014466.

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We investigated the distribution of heat shock protein 47 (hsp47) in cultured chicken embryonic chondrocytes and epiphyseal chondrocytes of tibial bones from 1-day-old to 6-week-old chickens. Northern blot and immunoblot analyses revealed that hsp47 exists in epiphyseal cartilage and cultured chondrocytes. Confocal laser immunofluorescence microscopy showed that hsp47 was localized mainly in the many granular structures found in the cytoplasm that contain Type II collagen. Epiphyseal cartilage and cultured chondrocytes were embedded in LR White resin and hsp47 was detected by protein A-immunog
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Rajpar, M. Helen, Ben McDermott, Louise Kung, et al. "Targeted Induction of Endoplasmic Reticulum Stress Induces Cartilage Pathology." PLoS Genetics 5, no. 10 (2009): e1000691. http://dx.doi.org/10.1371/journal.pgen.1000691.

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Yammani, R. R., J. Haywood, and R. F. Loeser. "Endoplasmic reticulum (ER) stress inhibits IGF-1 function in articular cartilage." Osteoarthritis and Cartilage 24 (April 2016): S180—S181. http://dx.doi.org/10.1016/j.joca.2016.01.355.

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Zhu, M., S. Zhou, Z. Huang, J. Wen, and H. Li. "Ca2+-Dependent Endoplasmic Reticulum Stress Regulates Mechanical Stress–Mediated Cartilage Thinning." Journal of Dental Research 95, no. 8 (2016): 889–96. http://dx.doi.org/10.1177/0022034516640206.

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5

Wang, Jiangxue, Yu Gao, Ying Hou, et al. "Evaluation on Cartilage Morphology after Intra-Articular Injection of Titanium Dioxide Nanoparticles in Rats." Journal of Nanomaterials 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/452767.

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Nanoscale wear particles would generate from orthopedic implants with nanoscale surface topography because of residual stress. In this study, the effect ofTiO2nanoparticles on articular cartilage was investigated by intra-articular injection in rats. Using contrast-enhanced high-resolution microcomputed tomography (micro-CT) technology, the decreased thickness of articular cartilage in distal femur was determined at 1, 7, 14, and 30 days after nanoparticle exposure. A strong linear correlation (r=0.928,P<0.0001) was observed with the results obtained by needle probe testing. After exposure
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Li, Huang, Xiang-Yu Zhang, Tuo-Jiang Wu, et al. "Endoplasmic Reticulum Stress Regulates Rat Mandibular Cartilage Thinning under Compressive Mechanical Stress." Journal of Biological Chemistry 288, no. 25 (2013): 18172–83. http://dx.doi.org/10.1074/jbc.m112.407296.

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Qu, Jining, Daigang Lu, Hua Guo, Wusheng Miao, Ge Wu, and Meifen Zhou. "PFKFB3 modulates glycolytic metabolism and alleviates endoplasmic reticulum stress in human osteoarthritis cartilage." Clinical and Experimental Pharmacology and Physiology 43, no. 3 (2016): 312–18. http://dx.doi.org/10.1111/1440-1681.12537.

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Horky, D., and F. Tichy. "Submicroscopic structure of canine articular cartilage." Veterinární Medicína 49, No. 6 (2012): 207–16. http://dx.doi.org/10.17221/5697-vetmed.

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Canine articular cartilage was studied in male dogs at age 1, 4, 5 and 8 years. Samples collected from four hip joints and two humeral joints in each age category were processed by standard methods to be examined by scanning and transmission electron microscopy. The cartilage of both joints was similar in structure. In the superficial cartilage layer of one-year-old animals, individual spindle-shaped chondrocytes in the extracellular matrix were, together with associated collagen fibrils, located parallel to the surface. When viewed by scanning electron microscopy, they were distinctly promine
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Yuan, Xiaoliang, Haiqing Liu, Linfu Li, et al. "The Roles of Endoplasmic Reticulum Stress in the Pathophysiological Development of Cartilage and Chondrocytes." Current Pharmaceutical Design 23, no. 11 (2017): 1693–704. http://dx.doi.org/10.2174/1381612822666161025152423.

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Xu, Ting, Zhiyuan Gu, Huiling Wu, Hua Yao, and Guohua Wang. "Expression of endoplasmic reticulum stress protein in rabbit condyle cartilage following anterior disk displacement." Journal of Oral Pathology & Medicine 47, no. 6 (2018): 606–12. http://dx.doi.org/10.1111/jop.12715.

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Dissertations / Theses on the topic "Endoplasmic reticulum. Bones Cartilage"

1

Chan, Cheuk-wing Wilson. "ER stress in the pathogenesis of osteochondrodysplasia." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085192.

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Chan, Cheuk-wing Wilson, and 陳卓榮. "ER stress in the pathogenesis of osteochondrodysplasia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085192.

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Tan, Zhijia, and 谭志佳. "Molecular analyses of chondrocyte differentiation and adaptation to ER stress." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/209435.

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Endochondral bone development depends on the progression of chondrocyte proliferation, hypertrophy and terminal differentiation, which requires precise transcriptional regulation and signaling coordination. Disturbance of this process would disrupt chondrocyte differentiation and lead to chondrodysplasias. In cells, a highly conserved mechanism, ER stress signaling, has been developed to sense the protein load and maintain the cellular homeostasis. In humans, mutations in COL10A1 induce ER stress and result in metaphyseal chondrodysplasia type Schmid (MCDS). Previous analysis of a MCDS mouse m
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4

Nugent, Ashleigh Elizabeth. "The Presence of Extracellular Matrix Alters the Chondrocyte Response to Endoplasmic Reticulum Stress." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1271375344.

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Pei, Lim-cho Steven, and 貝念祖. "Role(s) of p53/p63 in chondrocyte re-differentiation upon activation of ER stress." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/198926.

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Endoplasmic Reticulum (ER) stress signal is a cellular response to various insults including abnormal protein folding load, activating the unfolded protein response. Under severe ER stress, apoptosis will occur in most cell types. Interestingly, this does not happen in a disease model for Metaphyseal chondrodysplasia type Schmid (MCDS), where ER stress was activated in the hypertrophic zone of the growth plate where mutant collagen X proteins that cannot be folded correctly is expressed. Instead of normal progression from proliferating chondrocytes (PCs) to hypertrophic chondrocytes (HCs
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Lo, Ling-kit Rebecca. "ER-stress signaling and chondrocyte differentiation in mice." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B3861926X.

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Lo, Ling-kit Rebecca, and 羅令潔. "ER-stress signaling and chondrocyte differentiation in mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B3861926X.

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8

Saito, Motoo. "A VCP modulator, KUS121, as a promising therapeutic agent for post-traumatic osteoarthritis." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263546.

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You might also be interested in the extended bibliographies on the topic 'Endoplasmic reticulum. Bones Cartilage' for particular source types:
Journal articles
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