Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5

By Andrea Taddei, C. Giampietro, A. Conti, F. Orsenigo, F. Breviario, V. Pirazzoli, M. Potente, C. Daly, Stefanie Dimmeler, E. Dejana. Nature Cell Biology, 2008

647 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/09cd8221ac55795221a411ad10f914fe8ff44f97

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. E. Dejana
2. Peter Carmeliet
3. L. Sorokin
4. Peter C. Searson
5. P. Ratcliffe
6. G. Semenza
7. Rakesh K. Jain
8. W. Kaelin

In Molecular Biology

1. E. Dejana
2. M. Lampugnani
3. B. Engelhardt
4. L. Sorokin
5. Peter Carmeliet
6. Peter C. Searson
7. Julián Aragonés
8. P. Ratcliffe

In Neurology

1. E. Dejana
2. Amanda F. Levy
3. Mao Ye
4. Peter C. Searson
5. Jeffrey D. Rothstein
6. B. Engelhardt
7. D. Bergles
8. Andrew D. Wong

Citations in the corpus

• Tight junctions at the blood brain barrier: physiological architecture and disease-associated dysregulation (2012, neutral): “(a) The basal lamina protein agrin increases claudin-5 (Cld5) and occludin expression [92]; (b) Aquaporin-4 density, regulated by agrin, stabilizes TJ complexes through ZO-1 expression [93]; (c) β1-integrin engagement stabilizes Cld5 localization at the TJ [94]; (d) astrocyte/pericyte-secreted TGF-β”
• The blood-brain barrier: an engineering perspective (2013, background): “For example, evidence suggests that VE-cadherin at adherens junctions upregulates the gene encoding the tight junction protein claudin-5 (Dejana, 2004; Taddei et al., 2008).”
• Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological conditions. (2013, neutral): “tions induces claudin-5 expression (Taddei et al., 2008).”
• Heterozygous Deficiency of PHD2 Restores Tumor Oxygenation and Inhibits Metastasis via Endothelial Normalization (2009, positive): “Indeed, VE-cadherin inhibits EC proliferation and apoptosis and tightens the barrier (Carmeliet et al., 1999; Taddei et al., 2008).”
• The blood–brain and the blood–cerebrospinal fluid barriers: function and dysfunction (2009, background): “However, very recent studies demonstrate that adhesive interactions of VE-cadherin promote claudin-5 expression by preventing the nuclear accumulation of the transcriptional regulators, FoxO1 and β-catenin [25].”
• The blood-brain barrier in brain homeostasis and neurological diseases. (2009, neutral): “More recently, the functional relationship between AJs and TJs was further documented by the demonstration that VE-cadherin at AJs upregulates the expression of claudin-5 at TJs, through activation of the transcription factor Fox01 [62].”