Ignet

Gene Information

Gene symbol: ENG

Gene name: endoglin

HGNC ID: 3349

Synonyms: END, HHT1, CD105

Related Genes

#	Gene Symbol	Number of hits
1	ACD	1 hits
2	ACTC1	1 hits
3	ACVRL1	1 hits
4	ALB	1 hits
5	ALCAM	1 hits
6	ANPEP	1 hits
7	BMP7	1 hits
8	CD14	1 hits
9	CD34	1 hits
10	CD44	1 hits
11	CDH5	1 hits
12	CSF3	1 hits
13	HIF1A	1 hits
14	HMGB1	1 hits
15	INHBE	1 hits
16	INS	1 hits
17	ITGAL	1 hits
18	ITGB1	1 hits
19	KDR	1 hits
20	KIT	1 hits
21	LGALS13	1 hits
22	MKI67	1 hits
23	MSC	1 hits
24	NANOG	1 hits
25	NES	1 hits
26	NT5E	1 hits
27	PECAM1	1 hits
28	PGF	1 hits
29	PLXNA2	1 hits
30	POU5F1	1 hits
31	PROM1	1 hits
32	PTPRC	1 hits
33	SETD2	1 hits
34	TGFB1	1 hits
35	TGFB3	1 hits
36	TGFBR1	1 hits
37	THY1	1 hits
38	VEGFA	1 hits
39	VIM	1 hits

Related Sentences

#	PMID	Sentence
1	16202216	In an additional cohort of 11 patients with advanced proliferative retinopathy and 23 control subjects, CD105 and VEGF were measured in the vitreous.
2	17460896	The epithelial cells expressed PDX-1, PCNA, CK-7, CK-19, Nestin, Glut2, and Vimentin, but Insulin was undetected.
3	17460896	The cells expressed CD29, CD44, and CD166, but did not express CD11a, CD14, CD34, CD45, CD90, CD105, and CD117.
4	17549301	Biphasic effect of pioglitazone on isolated human endothelial progenitor cells: involvement of peroxisome proliferator-activated receptor-gamma and transforming growth factor-beta1.
5	17549301	We evaluated the effects of the anti-diabetic drug pioglitazone on human EPC function and the involvement of PPAR-gamma and TGF-beta1.
6	17549301	EPCs in culture were characterized at day 7 by the development of colony-forming units (CFUs) and flow cytometry assessment of differentiation marker (DiI-ac-LDL/lectin, KDR and CD31).
7	17549301	Treatment with pioglitazone for 72 hours increased the number of EPC-CFUs, DiI-ac-LDL(+)/lectin(+), CD31(+) and KDR(+) EPCs at 1 microM but not at 10 microM.
8	17549301	Indeed, pioglitazone increased EPC adhesion in flow at 1 microM, an effect prevented by PPAR-gamma and beta2-integrin blockade.
9	17549301	As determined by ELISA, pioglitazone induced a persistent increase in TGF-beta1 secretion only at 10 microM when a significantly elevated expression of endoglin, the accessory receptor for TGF-beta1, was also observed.
10	17901402	Transcripts for insulin, glucagon, and somatostatin in recovered ECC grafts increased with time in vivo, reaching levels approximately 1% of those in adult islets.
11	17901402	We show that hIPCs are mesenchymal stromal cells (MSCs) that adhere to plastic, express CD73, CD90, and CD105, and can differentiate in vitro into adipocytes, chondrocytes, and osteocytes.
12	17901402	Moreover, we find a minor population of CD105(+)/CD73(+)/CD90(+) cells in adult human islets (prior to incubation in vitro) that express insulin mRNA at low levels.
13	17901402	Transcripts for insulin, glucagon, and somatostatin in recovered ECC grafts increased with time in vivo, reaching levels approximately 1% of those in adult islets.
14	17901402	We show that hIPCs are mesenchymal stromal cells (MSCs) that adhere to plastic, express CD73, CD90, and CD105, and can differentiate in vitro into adipocytes, chondrocytes, and osteocytes.
15	17901402	Moreover, we find a minor population of CD105(+)/CD73(+)/CD90(+) cells in adult human islets (prior to incubation in vitro) that express insulin mRNA at low levels.
16	18366008	Its expression is increased by the hypoxia inducible factor 1 (HIF-1), a potent stimulator of VEGF expression.
17	18366008	The relative hypoxic environment in which foetal lung develops favours HIF-1 dependent gene expression, including the endoglin and VEGF ones.
18	18366008	In case of alveolar capillary dysplasia (ACD) or macrosomy associated with maternal diabetes, endoglin expression was restricted to peri-bronchial vessels; no immunoreaction was encountered in foetuses with IUGR (intra-uterine growth restriction) or massive pulmonary haemorrhage.
19	18366008	Its expression is increased by the hypoxia inducible factor 1 (HIF-1), a potent stimulator of VEGF expression.
20	18366008	The relative hypoxic environment in which foetal lung develops favours HIF-1 dependent gene expression, including the endoglin and VEGF ones.
21	18366008	In case of alveolar capillary dysplasia (ACD) or macrosomy associated with maternal diabetes, endoglin expression was restricted to peri-bronchial vessels; no immunoreaction was encountered in foetuses with IUGR (intra-uterine growth restriction) or massive pulmonary haemorrhage.
22	18854808	The most promising biochemical markers, to date, are placenta protein 13 (PP-13) as well as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng).
23	19395281	Endoglin is an accessory receptor molecule that, in association with transforming growth factor beta (TGF-beta) family receptors Types I and II, binds TGF-beta1, TGF-beta3, activin A, bone morphogenetic protein (BMP)-2 and BMP-7, regulating TGF-beta dependent cellular responses.
24	19539633	Endothelial cells are unique in expressing a second TGFbeta type I receptor, Alk1, as well as the co-receptor, endoglin which increases the affinity of the ligand to Alk1.
25	19539633	In differentiated blood outgrowth endothelial cells from normal subjects Alk1 and endoglin are constitutively expressed.
26	19539633	Incubation with high glucose (HG) and glycated albumin (gAlb) induces Alk5 and raises TGFbeta secretion 3-fold without affecting Alk1 or endoglin levels.
27	19539633	This diabetic milieu accelerates cell proliferation, at least in part, through TGFbeta/Alk1-smad1/5 and probably involving VEGF as well as pro-migratory MMP2 downstream of Alk1.
28	19539633	In contrast, HG/gAlb also increases caspase-3 activity (suggesting increased apoptosis) in part but not entirely using a TGFbeta/Alk5-smad2/3 pathway.
29	19539633	The findings support pleiotropy of TGFbeta in endothelial cells including proliferative effects (through Alk1-smad1/5) and pro-apoptotic signals (through Alk5-smad2/3).
30	19539633	Endothelial cells are unique in expressing a second TGFbeta type I receptor, Alk1, as well as the co-receptor, endoglin which increases the affinity of the ligand to Alk1.
31	19539633	In differentiated blood outgrowth endothelial cells from normal subjects Alk1 and endoglin are constitutively expressed.
32	19539633	Incubation with high glucose (HG) and glycated albumin (gAlb) induces Alk5 and raises TGFbeta secretion 3-fold without affecting Alk1 or endoglin levels.
33	19539633	This diabetic milieu accelerates cell proliferation, at least in part, through TGFbeta/Alk1-smad1/5 and probably involving VEGF as well as pro-migratory MMP2 downstream of Alk1.
34	19539633	In contrast, HG/gAlb also increases caspase-3 activity (suggesting increased apoptosis) in part but not entirely using a TGFbeta/Alk5-smad2/3 pathway.
35	19539633	The findings support pleiotropy of TGFbeta in endothelial cells including proliferative effects (through Alk1-smad1/5) and pro-apoptotic signals (through Alk5-smad2/3).
36	19539633	Endothelial cells are unique in expressing a second TGFbeta type I receptor, Alk1, as well as the co-receptor, endoglin which increases the affinity of the ligand to Alk1.
37	19539633	In differentiated blood outgrowth endothelial cells from normal subjects Alk1 and endoglin are constitutively expressed.
38	19539633	Incubation with high glucose (HG) and glycated albumin (gAlb) induces Alk5 and raises TGFbeta secretion 3-fold without affecting Alk1 or endoglin levels.
39	19539633	This diabetic milieu accelerates cell proliferation, at least in part, through TGFbeta/Alk1-smad1/5 and probably involving VEGF as well as pro-migratory MMP2 downstream of Alk1.
40	19539633	In contrast, HG/gAlb also increases caspase-3 activity (suggesting increased apoptosis) in part but not entirely using a TGFbeta/Alk5-smad2/3 pathway.
41	19539633	The findings support pleiotropy of TGFbeta in endothelial cells including proliferative effects (through Alk1-smad1/5) and pro-apoptotic signals (through Alk5-smad2/3).
42	20158462	After long term cryo-preservation hTGSCs expressed surface antigens CD29, CD73, CD90, CD105, and CD166, but not CD34, CD45 or CD133, which was typical for non-frozen hTGSCs.
43	20948996	Soluble fms-Like tyrosine kinase 1 (sFlt1), endoglin and placental growth factor (PlGF) in preeclampsia among high risk pregnancies.
44	21099303	Human umbilical cord matrix stem cells (hUCMSCs) were found to express CD29, CD44, CD73, CD90, CD105, smooth muscle actin, nestin, vimentin, proliferation marker Ki67 and embryonic markers Oct4, SSEA4.
45	21099303	These were found to be negative for CD33, CD34, CD45 and HLA DR.
46	21099303	Real time qPCR analysis of newly generated islets further demonstrated abundance of Pdx-1, Ngn3, insulin, glucagon and somatostatin transcripts.
47	21099310	In these clusters the expression of insulin, glucagon, and somatostatin genes is induced.
48	21099310	Human IPC lack expression of Von Willebrand Factor, CD31, CD34, CD45, and CK19 and CA19.9, demonstrating that hIPC are neither of hematopoietic, endothelial, nor of ductal origin.
49	21099310	The mesenchymal stem cells (MSC) markers CD105, CD90, CD73, CD44, CD29, and CD13 are expressed, as well as nestin and vimentin.
50	21099310	Also hIPC express the pericyte markers CD146, NG2, αSMA and PDGF-Rβ.
51	21099310	Immunoflowcytometry revealed that human islets contain 2.0 ± 0.8% of CD105/CD90 double-positive cells.
52	21099310	In these clusters the expression of insulin, glucagon, and somatostatin genes is induced.
53	21099310	Human IPC lack expression of Von Willebrand Factor, CD31, CD34, CD45, and CK19 and CA19.9, demonstrating that hIPC are neither of hematopoietic, endothelial, nor of ductal origin.
54	21099310	The mesenchymal stem cells (MSC) markers CD105, CD90, CD73, CD44, CD29, and CD13 are expressed, as well as nestin and vimentin.
55	21099310	Also hIPC express the pericyte markers CD146, NG2, αSMA and PDGF-Rβ.
56	21099310	Immunoflowcytometry revealed that human islets contain 2.0 ± 0.8% of CD105/CD90 double-positive cells.
57	21547696	Isolation of Oct4+, Nanog+ and SOX2- mesenchymal cells from peripheral blood of a diabetes mellitus patient.
58	21547696	They expressed embryonic stem cell pluripotency markers Nanog and Oct 4 as well as mesenchymal markers CD105 and CD13, and they lacked expression of hematopoietic marker CD45.
59	23118492	The aim of this study was to measure the levels of high-mobility group box-1 (HMGB1) in the vitreous fluid from patients with proliferative diabetic retinopathy (PDR) and to correlate its levels with clinical disease activity and the levels of vascular endothelial growth factor (VEGF), the angiogenic cytokine granulocyte-colony-stimulating factor (G-CSF), the endothelial cell angiogenic markers soluble vascular endothelial-cadherin (sVE-cadherin), and soluble endoglin (sEng).
60	23118492	HMGB1, VEGF, sVE-cadherin, and sEng levels were significantly higher in PDR patients than in nondiabetics (P = 0.008; <0.001; <0.001; 0.003, resp.).
61	23118492	Our findings suggest that HMGB1, VEGF, sVE-cadherin and sEng regulate the angiogenesis in PDR.
62	23255220	Cultured islets exhibited reduced expression of EC markers (VEGFR2, VE-cadherin and CD31), which was associated with diminished but sustained expression of endoglin a marker of both ECs and MSCs.
63	23255220	In vitro coculture of microvascular ECs with endoglin-positive, CD31-negative islet MSCs reduced VEGFR2 protein expression, disrupted EC angiogenic behavior, and increased EC detachment.
64	23255220	EC:MSC cocultures showed enhanced Smad2 phosphorylation consistent with altered ALK5 signaling.
65	23255220	Thus, endoglin-expressing islet MSCs influence EC ALK5 signaling in vitro, which decreases EC viability, and changes in ALK5 activity in whole cultured islets contribute to islet EC loss.
66	23255220	Cultured islets exhibited reduced expression of EC markers (VEGFR2, VE-cadherin and CD31), which was associated with diminished but sustained expression of endoglin a marker of both ECs and MSCs.
67	23255220	In vitro coculture of microvascular ECs with endoglin-positive, CD31-negative islet MSCs reduced VEGFR2 protein expression, disrupted EC angiogenic behavior, and increased EC detachment.
68	23255220	EC:MSC cocultures showed enhanced Smad2 phosphorylation consistent with altered ALK5 signaling.
69	23255220	Thus, endoglin-expressing islet MSCs influence EC ALK5 signaling in vitro, which decreases EC viability, and changes in ALK5 activity in whole cultured islets contribute to islet EC loss.
70	23255220	Cultured islets exhibited reduced expression of EC markers (VEGFR2, VE-cadherin and CD31), which was associated with diminished but sustained expression of endoglin a marker of both ECs and MSCs.
71	23255220	In vitro coculture of microvascular ECs with endoglin-positive, CD31-negative islet MSCs reduced VEGFR2 protein expression, disrupted EC angiogenic behavior, and increased EC detachment.
72	23255220	EC:MSC cocultures showed enhanced Smad2 phosphorylation consistent with altered ALK5 signaling.
73	23255220	Thus, endoglin-expressing islet MSCs influence EC ALK5 signaling in vitro, which decreases EC viability, and changes in ALK5 activity in whole cultured islets contribute to islet EC loss.
74	23913471	There is an increased attention directed towards the role of angiogenic factors including vascular endothelial growth factor (VEGF) and anti-angiogenic factors including soluble endoglin (sEng) as contributors to diabetic microvascular complications including neuropathy.
75	23913471	In all groups, plasma VEGF, sEng and endothelin-1 (ET-1), nitric oxide and ET-1 mRNA were estimated.
76	23913471	Plasma levels of VEGF, sEng, ET-1 and nitric oxide were significantly elevated in diabetic patients (Groups I and II) compared with healthy control subjects, with a higher increase in their levels in patients with DPN compared with diabetic patients without peripheral neuropathy.
77	23998797	FACS analysis of CD73, CD90, and CD105 expression showed no significant difference among examined passages; however, the mRNA expression levels of pluripotent markers, Oct4 and Nanog, were significantly decreased at higher passages.