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Collectively, these data indicate that Syn4 suppresses the cellular proliferation during neurogenesis and is crucial for the formation of caudal primary axons during zebrafish embryogenesis.
We show here that sdc2,sdc3 and sdc4 are expressed in the zebrafish embryonic brain during the major period of axon growth. These genes show differing expression patterns in the brain which provides putative insights into their functional specificity.
cell adhesion properties of syndecan-4 are consistent across the vertebrate spectrum and reflect an early acquisition of specialization after syndecan gene duplication events at the invertebrate/early chordate boundary
Dynamic changes in syndecan-4- and glypican-1-positive satellite cells indicate that they are differentially expressed during myogenesis.
The cytoplasmic domain of syndecan-4 is required for cell migration and RhoA activation in skeletal muscle satellite cells.
results suggest that syndecan-4 and its side chains play important roles in regulating FAK activity, and PKCalpha and beta1-integrin cell membrane localization, but not cell apoptosis and vinculin-containing focal adhesion formation in satellite cells
These data suggested that expression of the myogenic regulatory transcription factors are dependent upon expression of glypican-1 and syndecan-4 during satellite cell proliferation and differentiation, and Pax7 expression is influenced by glypican-1.
syndecan-1, syndecan-4, or glypican-1 differentially affect the processes of turkey muscle cell proliferation and differentiation, and can regulate these developmental stages in an FGF2-independent manner
SDC4 gene silencing affects cell Epithelial Mesenchymal Transition and apoptosis of papillary thyroid cancer through the Wnt/beta-catenin signaling pathway.
Regulation of vascular smooth muscle cell calcification by syndecan-4/FGF-2/PKCalpha signalling and cross-talk with TGF-beta1.
Downregulation of SDC-4 inhibited FGF signaling through the blockade of ERK1/2 and PI3K/Akt/mTOR activation, thus suppressing cell proliferation and migration.
studies are required to show if syndecan-4 concentrations can be marker for prognosis assessment or disease progression
Data provide evidence that SDC4 plays important roles in normal physiology of intervertebral disc and cartilage through controlling growth factor signaling and matrix homeostasis. However, several studies to date clearly show that in diseased joints, SDC4 and inflammatory cytokines IL-1beta and TNF-alpha form a positive feedback loop, wherein they control each other's expression and/or activity. [review]
This study demonstrates that the shedding of synd4 from Endothelial progenitor cells (EPCs) plays a key role in advanced glycation end products-mediated dysfunction of EPC migration and homing.
the Ser179Glu mutant of SDC-4 binds strongly Tiam1, a Rac1-GEF reducing Rac1-GTP by 3-fold in MCF-7 breast adenocarcinoma cells.
Syndecan 4 is the biomarker independently distinguishing Heart Failure with preserved ejection fraction and Heart Failure with reduced ejection fraction.
The upregulation of syndecan-4 in the eutopic endometrium of endometriosis patients may facilitate the pathogenetic process by promoting invasive cell growth via Rac1, MMP3, and ATF-2.
Sdc4 has been identified as a mycobacterial attachment receptor on alveolar epithelial cells.
Study has demonstrated that SDC-4 expression was increased in sera and skin of atopic dermatitis (AD) patients, suggesting that SDC-4 may contribute to the development of AD.
the present study demonstrated that synd4 was involved in the chemotactic migration of ECs in vitro and in vivo.
results suggest that SDC4 alleles affect lipid profile in elderly subjects and may in part mediate the link between LDL-C and longevity.
Synd4 shedding is a molecular pathological alteration in the development and maintenance of inflammation-associated atrial fibrillation.
Syndecan-4 is essential for transmitting the mechanotransduction signals via activation of PKC-alpha and is important for tumor cells spreading, assembly of actin cytoskeleton and cell contractility.
demonstrate that HER2 is captured via a site, comprised of amino acids 210-240, in the extracellular domain of human Sdc1, and EGFR is captured via an extracellular site comprised of amino acids 87-131 in human Sdc4
Data indicate that the extracellular and cytoplasmic domains of syndecans 1/2/3/4 are intrinsically disordered regions.
Dynamic catch of a Thy-1-integrin alpha5beta1+syndecan-4 trimolecular complex explains extraordinary cancer cell adhesion to the vascular endothelium.
Syndecan-4 polymorphisms were associated with essential hypertension, body mass index, and coronary artery disease prevalence in the Tampere adult population cardiovascular risk study.
No association was found with SDC4 and breast cancer.
Results suggest that syndecan-4 functions as a reservoir for promyostatin regulating the local bioavailability of mature myostatin.
These data indicate that the HSPG syndecan-4 plays important role(s) in the insulin secretory response.
Endothelial dysfunction induces the expression of syndecan-4 via activation of the NF-kappaB pathway. Syndecan-4 is shed to a greater amount because of increased oxidative stress in dysfunctional endothelial cells and the release of the syndecan-4 ectodomain leads to tubulointerstitial fibrosis.
SDC4 antagonizes the activation of RIG-I in a CYLD-mediated deubiquitination-dependent process, thereby balancing antiviral signalling to avoid deleterious effects on host cells.
Cell-extracellular matrix and cell-cell adhesion are linked by syndecan-4.
Syndecan-4 is essential for the compensated hypertrophy and the maintenance of cardiac function during the process of heart failure following pressure overload.
Syndecan-4 therapy also induces a marked immunomodulation in the tissues, increasing the polarization of macrophages toward the M2 phenotype.
SDC4 thus controls flow-induced lymphatic endothelial cell polarization via regulation of VANGL2 expression.
loss of N-sulfation leads to the disruption of the pattern of distribution of Sdc-4 within the glomeruli of Ndst1-/- mutants
Synd4 shedding from vascular endothelial cells played an important role in the diabetes-related impairment of angiogenesis.
Data show that differentiative switches between bronchiolar progenitors and club cells are under the Nrf2-mediated control of SLPI and syndecan 4.
Shedding of syndecan-4 promotes immune cell recruitment and mitigates cardiac dysfunction after lipopolysaccharide challenge in mice.
SDC4 plays an important role in asthma induction. Disturbed SDC4 signalling leads to an impaired motility and directional migration of antigen-presenting dendritic cells.
Syndecan-4 exerts a dual role in collagen cross-linking, one involving its cytosolic domain and calcineurin/nuclear factor of activated T-cells signalling leading to collagen
Locally generated Sdc4 may play a role in regulating TRPC6 channels, and may contribute to glomerular pathology.
Sdc4 contributes to the development of collagen induced arthritis by promoting germinal center formation and autoantibody production through its regulation of SDF-1-mediated B cell migration.
binding interaction between syndesmos and syn4(cyto) was characterized as a low-affinity interaction (Kd = 62 muM) by surface plasmon resonance and nuclear magnetic resonance
Syndecan-4 mediates porcine respiratory and reproductive syndrome virus entry by interacting with EGFR.
changing placental expression indicates possible involvement in fetomaternal communication and placental maturation
TGF-beta1 modulates the expression of syndecan-4 in cultured vascular endothelial cells in a biphasic manner.
Syndecan-4 acts as a central mediator that bridges fibronectin, integrin and intracellular components (actin and vinculin) and once silenced, the cytoskeleton protein network is disrupted, highlighting Syn4 relevance for balanced cell behavior.
Findings suggest that syndecan-4 may be involved in acquisition of resistance to detachment-induced cell death (anoikis resistance) in endothelial cells, thus contributing to cell transformation.
The protein encoded by this gene is a transmembrane (type I) heparan sulfate proteoglycan that functions as a receptor in intracellular signaling. The encoded protein is found as a homodimer and is a member of the syndecan proteoglycan family. This gene is found on chromosome 20, while a pseudogene has been found on chromosome 22.
, ryudocan core protein
, syndecan 4 like
, heparan sulfate proteoglycan
, syndecan 4 (amphiglycan, ryudocan)
, ryudocan amphiglycan
, syndecan proteoglycan 4
, Ryudocan/syndecan 4