Syndecan-3 is one of four identified members of a family of transmembrane proteoglycans (the syndecans) that possess highly similar cytoplasmic and transmembrane domains and may function as extracellular matrix receptors and/or low affinity receptors for signaling molecules such as FGF. We previously reported the cloning of a partial cDNA for chicken syndecan-3. Here we report the isolation of a syndecan-3 cDNA containing additional 5' sequence which includes a potential methionine start codon and putative signal sequence. In vitro translation of syndecan-3 cDNA in the presence and absence of microsomes suggests that the putative signal sequence is functional, suggesting that the cDNA may encompass the full coding sequence. We also identify syndecan-3 as a heparan sulfate proteoglycan and report its expression pattern during chicken embryogenesis using polyclonal antibodies raised against a recombinant fusion protein. We detect abundant syndecan-3 expression in the developing brain and neural tube, including a striking expression in the floor plate of the neural tube. During limb development, syndecan-3 is expressed in the distal mesenchymal cells of the limb bud which are undergoing outgrowth in response to the apical ectodermal ridge. Syndecan-3 is also transiently expressed during the formation of the precartilage condensations of the skeletal elements of the limb and subsequently in association with the differentiating osteoblasts of the periosteum. Expression is also observed in several areas of tissue interactions including the developing lens, otic vesicle, genital ridge, sclerotome, and feather buds.
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http://dx.doi.org/10.1006/dbio.1995.1093 | DOI Listing |
J Dairy Sci
December 2024
College of Coastal Agricultural Sciences, Guangdong Ocean University, Zhanjiang 524088, China; The Key Laboratory of Animal Resources and Breed Innovation in Western Guangdong Province, Zhanjiang 524088, China. Electronic address:
J Biochem
September 2024
Department of Molecular Nutrition, CSIR-Central Food Technological Research Institute, Cheluvamba Mansion, KRS Road, Mysore 570020, Karnataka, India.
Erythrocytes are important vascular components that play vital roles in maintaining vascular homeostasis, in addition to carrying oxygen. Previously, we reported that the changes in the internal milieu (e.g.
View Article and Find Full Text PDFThe sleep-wake cycle regulates interstitial fluid and cerebrospinal fluid (CSF) tau levels in both mouse and human by mechanisms that remain unestablished. Here, we reveal a novel pathway by which wakefulness increases extracellular tau levels in mouse and humans. In mice, higher body temperature (BT) associated with wakefulness and sleep deprivation increased CSF tau.
View Article and Find Full Text PDFMol Cell Neurosci
June 2024
Stem Cell and Neurogenesis Group, Genomics Research Centre, Centre for Genomics and Personalised Health, School of Biomedical Sciences, Queensland University of Technology (QUT), 60 Musk Ave., Kelvin Grove, Queensland 4059, Australia; Centre for Biomedical Technologies, Queensland University of Technology (QUT), 60 Musk Ave., Kelvin Grove, QLD 4059, Australia; ARC Training Centre for Cell and Tissue Engineering Technologies, Queensland University of Technology (QUT), Australia; Max Planck Queensland Centre for the Materials Sciences of Extracellular Matrices, Queensland University of Technology (QUT), Australia. Electronic address:
Neurological disorders impact around one billion individuals globally (15 % approx.), with significant implications for disability and mortality with their impact in Australia currently amounts to 6.8 million deaths annually.
View Article and Find Full Text PDFCells
March 2024
Department of Health Sciences and Sport Medicine, Hungarian University of Sports Science, 1123 Budapest, Hungary.
Amyotrophic lateral sclerosis (ALS) is a mysterious lethal multisystem neurodegenerative disease that gradually leads to the progressive loss of motor neurons. A recent non-contact dying-back injury mechanism theory for ALS proposed that the primary damage is an acquired irreversible intrafusal proprioceptive terminal Piezo2 channelopathy with underlying genetic and environmental risk factors. Underpinning this is the theory that excessively prolonged proprioceptive mechanotransduction under allostasis may induce dysfunctionality in mitochondria, leading to Piezo2 channelopathy.
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