Ignet

Gene Information

Gene symbol: SDC4

Gene name: syndecan 4

HGNC ID: 10661

Synonyms: SYND4, amphiglycan, ryudocan

Related Genes

#	Gene Symbol	Number of hits
1	ACTN4	1 hits
2	ADAM17	1 hits
3	BGN	1 hits
4	CDH17	1 hits
5	COL1A1	1 hits
6	DCN	1 hits
7	FBN1	1 hits
8	GPC1	1 hits
9	HSPG2	1 hits
10	JUP	1 hits
11	NFATC1	1 hits
12	PRKCA	1 hits
13	PTPRO	1 hits
14	RAC1	1 hits
15	RHOA	1 hits
16	RHOD	1 hits
17	SDC1	1 hits
18	TJP1	1 hits
19	TNF	1 hits
20	TRPC6	1 hits
21	VCAN	1 hits
22	VCL	1 hits

Related Sentences

#	PMID	Sentence
1	9434070	Syndecan-4, glypican-1 and biglycan were all expressed in normal glomeruli, whereas syndecan-1, perlecan and versican mRNAs were confined to the papillary area.
2	9434070	By hybridizing adjacent sections with a probe for the podocyte-specific PTPase GLEPP-1, the glomerular cells containing mRNA for syndecan-4 and glypican-1 could be identified as podocytes, whereas the cells expressing biglycan were identified as mesangial cells.
3	9434070	The constitutive expression of syndecan-4, glypican-1 and biglycan in glomerular cells points to a role for these polyanionic molecules in maintaining the integrity of the glomerular filtration barrier.
4	9434070	Syndecan-4, glypican-1 and biglycan were all expressed in normal glomeruli, whereas syndecan-1, perlecan and versican mRNAs were confined to the papillary area.
5	9434070	By hybridizing adjacent sections with a probe for the podocyte-specific PTPase GLEPP-1, the glomerular cells containing mRNA for syndecan-4 and glypican-1 could be identified as podocytes, whereas the cells expressing biglycan were identified as mesangial cells.
6	9434070	The constitutive expression of syndecan-4, glypican-1 and biglycan in glomerular cells points to a role for these polyanionic molecules in maintaining the integrity of the glomerular filtration barrier.
7	9434070	Syndecan-4, glypican-1 and biglycan were all expressed in normal glomeruli, whereas syndecan-1, perlecan and versican mRNAs were confined to the papillary area.
8	9434070	By hybridizing adjacent sections with a probe for the podocyte-specific PTPase GLEPP-1, the glomerular cells containing mRNA for syndecan-4 and glypican-1 could be identified as podocytes, whereas the cells expressing biglycan were identified as mesangial cells.
9	9434070	The constitutive expression of syndecan-4, glypican-1 and biglycan in glomerular cells points to a role for these polyanionic molecules in maintaining the integrity of the glomerular filtration barrier.
10	16622173	We found that podocytes produce versican, syndecan-1, decorin, and biglycan together with the previously known PG syndecan-4, glypican, and perlecan.
11	16622173	PAN treatment downregulated the mRNA and the protein expression of both versican (by 24 +/- 6%, P < 0.01, for mRNA and by 50% for protein) and perlecan (by 14 +/- 5%, P < 0.05, for mRNA and by 50% for protein).
12	16622173	Steroid treatment decreased perlecan (by 24 +/- 3%, P < 0.01) and syndecan-1 expression (by 30 +/- 4%, P < 0.01) but increased the expression of decorin 2.5-fold.
13	20463653	Protein kinase Cα, a signaling molecule bound to and activated by syndecan-4, showed a fourfold increase in membrane localization-activation than that seen in control cells.
14	22155451	The proteoglycan syndecan 4 regulates transient receptor potential canonical 6 channels via RhoA/Rho-associated protein kinase signaling.
15	23338211	Other cell-matrix adhesion receptors expressed by podocytes include the integrins α2β1 and αvβ3, α-dystroglycan, syndecan-4 and type XVII collagen.
16	24190885	Retinal pigmented epithelial (RPE) cells that expressed high levels of E-cadherin and had cell-cell junctions rich in zona occludens (ZO)-1, β-catenin and heparan sulfate, required syndecan-4 but not fibronectin or protein kinase C α (PKCα) to assemble extracellular matrix (fibrillin microfibrils and perlecan).
17	24190885	In contrast, RPE cells that strongly expressed mesenchymal smooth muscle α-actin but little ZO-1 or E-cadherin, required fibronectin (like fibroblasts) and PKCα, but not syndecan-4.
18	24190885	TGFβ, which stimulates epithelial-mesenchymal transition, altered gene expression and overcame the dependency on syndecan-4 for microfibril deposition in epithelial RPE cells, whereas blocking cadherin interactions disrupted microfibril deposition.
19	24190885	Renal podocytes had a transitional phenotype with pericellular β-catenin but little ZO-1; they required syndecan-4 and fibronectin for efficient microfibril deposition.
20	24190885	Retinal pigmented epithelial (RPE) cells that expressed high levels of E-cadherin and had cell-cell junctions rich in zona occludens (ZO)-1, β-catenin and heparan sulfate, required syndecan-4 but not fibronectin or protein kinase C α (PKCα) to assemble extracellular matrix (fibrillin microfibrils and perlecan).
21	24190885	In contrast, RPE cells that strongly expressed mesenchymal smooth muscle α-actin but little ZO-1 or E-cadherin, required fibronectin (like fibroblasts) and PKCα, but not syndecan-4.
22	24190885	TGFβ, which stimulates epithelial-mesenchymal transition, altered gene expression and overcame the dependency on syndecan-4 for microfibril deposition in epithelial RPE cells, whereas blocking cadherin interactions disrupted microfibril deposition.
23	24190885	Renal podocytes had a transitional phenotype with pericellular β-catenin but little ZO-1; they required syndecan-4 and fibronectin for efficient microfibril deposition.
24	24190885	Retinal pigmented epithelial (RPE) cells that expressed high levels of E-cadherin and had cell-cell junctions rich in zona occludens (ZO)-1, β-catenin and heparan sulfate, required syndecan-4 but not fibronectin or protein kinase C α (PKCα) to assemble extracellular matrix (fibrillin microfibrils and perlecan).
25	24190885	In contrast, RPE cells that strongly expressed mesenchymal smooth muscle α-actin but little ZO-1 or E-cadherin, required fibronectin (like fibroblasts) and PKCα, but not syndecan-4.
26	24190885	TGFβ, which stimulates epithelial-mesenchymal transition, altered gene expression and overcame the dependency on syndecan-4 for microfibril deposition in epithelial RPE cells, whereas blocking cadherin interactions disrupted microfibril deposition.
27	24190885	Renal podocytes had a transitional phenotype with pericellular β-catenin but little ZO-1; they required syndecan-4 and fibronectin for efficient microfibril deposition.
28	24190885	Retinal pigmented epithelial (RPE) cells that expressed high levels of E-cadherin and had cell-cell junctions rich in zona occludens (ZO)-1, β-catenin and heparan sulfate, required syndecan-4 but not fibronectin or protein kinase C α (PKCα) to assemble extracellular matrix (fibrillin microfibrils and perlecan).
29	24190885	In contrast, RPE cells that strongly expressed mesenchymal smooth muscle α-actin but little ZO-1 or E-cadherin, required fibronectin (like fibroblasts) and PKCα, but not syndecan-4.
30	24190885	TGFβ, which stimulates epithelial-mesenchymal transition, altered gene expression and overcame the dependency on syndecan-4 for microfibril deposition in epithelial RPE cells, whereas blocking cadherin interactions disrupted microfibril deposition.
31	24190885	Renal podocytes had a transitional phenotype with pericellular β-catenin but little ZO-1; they required syndecan-4 and fibronectin for efficient microfibril deposition.
32	24942878	Thus, we hypothesized that high glucose modifies TRPC6 channels via increased oxidative stress and syndecan-4 (SDC-4) in human podocytes.
33	24942878	TRPC6 and SDC-4 transcripts and protein expression were measured using RT-PCR and in-cell Western assay.
34	24942878	High D-glucose increased TRPC6 transcripts to 8.66±4.08 (p<0.05) and TRPC6 protein expression to 1.44±0.07 (p<0.05) without altering SDC-4 transcripts or protein expression.
35	24942878	Increased oxidative stress using peroxynitrite significantly increased TRPC6 transcripts to 4.29±1.26 (p<0.05) and TRPC6 protein expression to 1.28±0.05 (p<0.05) without altering SDC-4 transcripts or protein expression.
36	24942878	High glucose modifies TRPC6 channels and ROS production via SDC-4 in human podocytes.
37	24942878	Thus, we hypothesized that high glucose modifies TRPC6 channels via increased oxidative stress and syndecan-4 (SDC-4) in human podocytes.
38	24942878	TRPC6 and SDC-4 transcripts and protein expression were measured using RT-PCR and in-cell Western assay.
39	24942878	High D-glucose increased TRPC6 transcripts to 8.66±4.08 (p<0.05) and TRPC6 protein expression to 1.44±0.07 (p<0.05) without altering SDC-4 transcripts or protein expression.
40	24942878	Increased oxidative stress using peroxynitrite significantly increased TRPC6 transcripts to 4.29±1.26 (p<0.05) and TRPC6 protein expression to 1.28±0.05 (p<0.05) without altering SDC-4 transcripts or protein expression.
41	24942878	High glucose modifies TRPC6 channels and ROS production via SDC-4 in human podocytes.
42	24942878	Thus, we hypothesized that high glucose modifies TRPC6 channels via increased oxidative stress and syndecan-4 (SDC-4) in human podocytes.
43	24942878	TRPC6 and SDC-4 transcripts and protein expression were measured using RT-PCR and in-cell Western assay.
44	24942878	High D-glucose increased TRPC6 transcripts to 8.66±4.08 (p<0.05) and TRPC6 protein expression to 1.44±0.07 (p<0.05) without altering SDC-4 transcripts or protein expression.
45	24942878	Increased oxidative stress using peroxynitrite significantly increased TRPC6 transcripts to 4.29±1.26 (p<0.05) and TRPC6 protein expression to 1.28±0.05 (p<0.05) without altering SDC-4 transcripts or protein expression.
46	24942878	High glucose modifies TRPC6 channels and ROS production via SDC-4 in human podocytes.
47	24942878	Thus, we hypothesized that high glucose modifies TRPC6 channels via increased oxidative stress and syndecan-4 (SDC-4) in human podocytes.
48	24942878	TRPC6 and SDC-4 transcripts and protein expression were measured using RT-PCR and in-cell Western assay.
49	24942878	High D-glucose increased TRPC6 transcripts to 8.66±4.08 (p<0.05) and TRPC6 protein expression to 1.44±0.07 (p<0.05) without altering SDC-4 transcripts or protein expression.
50	24942878	Increased oxidative stress using peroxynitrite significantly increased TRPC6 transcripts to 4.29±1.26 (p<0.05) and TRPC6 protein expression to 1.28±0.05 (p<0.05) without altering SDC-4 transcripts or protein expression.
51	24942878	High glucose modifies TRPC6 channels and ROS production via SDC-4 in human podocytes.
52	24942878	Thus, we hypothesized that high glucose modifies TRPC6 channels via increased oxidative stress and syndecan-4 (SDC-4) in human podocytes.
53	24942878	TRPC6 and SDC-4 transcripts and protein expression were measured using RT-PCR and in-cell Western assay.
54	24942878	High D-glucose increased TRPC6 transcripts to 8.66±4.08 (p<0.05) and TRPC6 protein expression to 1.44±0.07 (p<0.05) without altering SDC-4 transcripts or protein expression.
55	24942878	Increased oxidative stress using peroxynitrite significantly increased TRPC6 transcripts to 4.29±1.26 (p<0.05) and TRPC6 protein expression to 1.28±0.05 (p<0.05) without altering SDC-4 transcripts or protein expression.
56	24942878	High glucose modifies TRPC6 channels and ROS production via SDC-4 in human podocytes.
57	26193076	Sdc4 ectodomain increased generation of reactive oxygen species (ROS), reduced activation of RhoA, increased activation of Rac1, increased nuclear abundance of NFATc1, and increased total β3-integrin.
58	26193076	The effects of Sdc4 ectodomain on cell-surface TRPC6 were blocked by the ROS quencher TEMPOL, and by the Rac1 inhibitor NSC-23766, but were not blocked by inhibition of calcineurin-NFATc1 signaling.
59	26193076	Moreover, effects of Sdc4 ectodomain on TRPC6, ROS generation, Rac1 and RhoA modulation, and NFATc1 activation were blocked by cilengitide, a selective inhibitor of outside-in signaling through αv-containing integrins.
60	26193076	Exposure to TNF, or serum from three patients with recurrent FSGS in relapse, increased shedding of podocyte Sdc4 ectodomains into the surrounding medium.
61	26193076	This was also observed after treating podocytes with the metalloproteinase ADAM17 or after overexpression of the Sdc4 core protein.
62	26193076	Sdc4 ectodomain increased generation of reactive oxygen species (ROS), reduced activation of RhoA, increased activation of Rac1, increased nuclear abundance of NFATc1, and increased total β3-integrin.
63	26193076	The effects of Sdc4 ectodomain on cell-surface TRPC6 were blocked by the ROS quencher TEMPOL, and by the Rac1 inhibitor NSC-23766, but were not blocked by inhibition of calcineurin-NFATc1 signaling.
64	26193076	Moreover, effects of Sdc4 ectodomain on TRPC6, ROS generation, Rac1 and RhoA modulation, and NFATc1 activation were blocked by cilengitide, a selective inhibitor of outside-in signaling through αv-containing integrins.
65	26193076	Exposure to TNF, or serum from three patients with recurrent FSGS in relapse, increased shedding of podocyte Sdc4 ectodomains into the surrounding medium.
66	26193076	This was also observed after treating podocytes with the metalloproteinase ADAM17 or after overexpression of the Sdc4 core protein.
67	26193076	Sdc4 ectodomain increased generation of reactive oxygen species (ROS), reduced activation of RhoA, increased activation of Rac1, increased nuclear abundance of NFATc1, and increased total β3-integrin.
68	26193076	The effects of Sdc4 ectodomain on cell-surface TRPC6 were blocked by the ROS quencher TEMPOL, and by the Rac1 inhibitor NSC-23766, but were not blocked by inhibition of calcineurin-NFATc1 signaling.
69	26193076	Moreover, effects of Sdc4 ectodomain on TRPC6, ROS generation, Rac1 and RhoA modulation, and NFATc1 activation were blocked by cilengitide, a selective inhibitor of outside-in signaling through αv-containing integrins.
70	26193076	Exposure to TNF, or serum from three patients with recurrent FSGS in relapse, increased shedding of podocyte Sdc4 ectodomains into the surrounding medium.
71	26193076	This was also observed after treating podocytes with the metalloproteinase ADAM17 or after overexpression of the Sdc4 core protein.
72	26193076	Sdc4 ectodomain increased generation of reactive oxygen species (ROS), reduced activation of RhoA, increased activation of Rac1, increased nuclear abundance of NFATc1, and increased total β3-integrin.
73	26193076	The effects of Sdc4 ectodomain on cell-surface TRPC6 were blocked by the ROS quencher TEMPOL, and by the Rac1 inhibitor NSC-23766, but were not blocked by inhibition of calcineurin-NFATc1 signaling.
74	26193076	Moreover, effects of Sdc4 ectodomain on TRPC6, ROS generation, Rac1 and RhoA modulation, and NFATc1 activation were blocked by cilengitide, a selective inhibitor of outside-in signaling through αv-containing integrins.
75	26193076	Exposure to TNF, or serum from three patients with recurrent FSGS in relapse, increased shedding of podocyte Sdc4 ectodomains into the surrounding medium.
76	26193076	This was also observed after treating podocytes with the metalloproteinase ADAM17 or after overexpression of the Sdc4 core protein.
77	26193076	Sdc4 ectodomain increased generation of reactive oxygen species (ROS), reduced activation of RhoA, increased activation of Rac1, increased nuclear abundance of NFATc1, and increased total β3-integrin.
78	26193076	The effects of Sdc4 ectodomain on cell-surface TRPC6 were blocked by the ROS quencher TEMPOL, and by the Rac1 inhibitor NSC-23766, but were not blocked by inhibition of calcineurin-NFATc1 signaling.
79	26193076	Moreover, effects of Sdc4 ectodomain on TRPC6, ROS generation, Rac1 and RhoA modulation, and NFATc1 activation were blocked by cilengitide, a selective inhibitor of outside-in signaling through αv-containing integrins.
80	26193076	Exposure to TNF, or serum from three patients with recurrent FSGS in relapse, increased shedding of podocyte Sdc4 ectodomains into the surrounding medium.
81	26193076	This was also observed after treating podocytes with the metalloproteinase ADAM17 or after overexpression of the Sdc4 core protein.
82	26936875	Immunostaining of glomeruli from mice whose podocytes were null for Ndst1 (Ndst1(-/-)) showed a disrupted pattern of localization for the cell surface proteoglycan, syndecan-4, and for α-actinin-4 compared with controls.
83	26936875	The pattern of immunostaining for synaptopodin and nephrin did not show as significant alterations.
84	26936875	Immunostaining in vitro for several markers for molecules involved in cell-matrix interactions showed that Ndst1(-/-) cells had decreased clustering of syndecan-4 and decreased recruitment of protein kinase-Cα, α-actinin-4, vinculin, and phospho-focal adhesion kinase to focal adhesions.
85	26936875	Immunostaining of glomeruli from mice whose podocytes were null for Ndst1 (Ndst1(-/-)) showed a disrupted pattern of localization for the cell surface proteoglycan, syndecan-4, and for α-actinin-4 compared with controls.
86	26936875	The pattern of immunostaining for synaptopodin and nephrin did not show as significant alterations.
87	26936875	Immunostaining in vitro for several markers for molecules involved in cell-matrix interactions showed that Ndst1(-/-) cells had decreased clustering of syndecan-4 and decreased recruitment of protein kinase-Cα, α-actinin-4, vinculin, and phospho-focal adhesion kinase to focal adhesions.