NCBI . NLM . NIH . GOV {
}
We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC5218530/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC5218530/. The analysis below is for the second page.
Title[redir]:
Angiopoietin receptor Tie2 is required for vein specification and maintenance via regulating COUP-TFII - PMC
Description:
Mechanisms underlying the vein development remain largely unknown. Tie2 signaling mediates endothelial cell (EC) survival and vascular maturation and its activating mutations are linked to venous malformations. Here we show that vein formation are ...
Title[redir]:
Angiopoietin receptor Tie2 is required for vein specification and maintenance via regulating COUP-TFII - PMC
Description:
Mechanisms underlying the vein development remain largely unknown. Tie2 signaling mediates endothelial cell (EC) survival and vascular maturation and its activating mutations are linked to venous malformations. Here we show that vein formation are ...
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What is the average monthly size of ncbi.nlm.nih.gov audience?
π Phenomenal Traffic: 5M - 10M visitors per month
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Keywords {π}
tie, mice, figure, doi, couptfii, deletion, analysis, venous, control, veins, vascular, development, data, tekiucko, cells, endothelial, article, tek, authors, akt, lymphatic, vein, expression, blood, mutant, pubmed, google, scholar, retina, shown, retinal, cell, formation, study, skin, protein, arterial, signaling, level, reviewer, pathway, vessels, tieiucko, supplement, pmc, gene, experiments, manuscript, mouse, interpretation,
Topics {βοΈ}
rabbit monoclonal anti-phospho-akt473 rabbit polyclonal anti-phospho-p56dok-2 ve-cadherin-creert2 mouse line mouse monoclonal anti-coup-tfii real-time rt-pcr revealed quantitative real-time rtβpcr funding statement rabbit polyclonal anti-p56dok-2 counterbalance vegfr2/mapk pathway counterbalance vegfr2/mapk signaling vegf-a-dependent arteriogenesis tekflox/β/ubc-creert2 neonatal mice ras-erk pathway downstream rabbit polyclonal anti-erk1/2 pmc beta search rabbit polyclonal anti-akt goat anti-mouse tie2 funding information tekflox/+/cdh5-creert2 littermate mice real-time rt-pcr goat anti-mouse dll4 goat anti-mouse ephb4 coup-tfii protein stability rat anti-mouse pecam-1 angiopoietin-1-dependent cell migration regulate coup-tfii expression wnt/Ξ²-catenin coup-tfii protein level stimulate tie2/akt pathway cell-autonomous effect resulting pi3k/akt signaling pathway long-term postnatal attenuation coup-tfii mrna level inhibit raf1-erk1/2 signaling coup-tfii/beta-actin ec-specific tek deletion fluorochrome-conjugated secondary antibodies ischemia-induced retinal neovascularization license information pmcid upregulating dll4/notch signaling abnormal arterial-venous alignment publisher site pdf definite genetic models increase coup-tfii level editorial decision letter tekβ/iecko mice resulted peer review follow tekβ/iecko mutant mice tek-/iecko mutant mice tie2-/iecko mutants compared
Questions {β}
- Do the authors claim to have achieved 100% deletion of Tie2 in these experiments or why are these images not showing the expected mosaic staining pattern resulting from partial recombination?
- Does loss of Tie2 lead to increased turnover of COUP-TFII?
- However, the embryos shown in the E panel seem considerably younger than the ones in the D panel?
- Is this solely due to different recombination efficacies of the different drivers or would this difference raise the question whether endothelial cell autonomous effects may not be the only cause of defective vein development in Tie2-deficient mice?
- This has a bearing also on the (lack of?
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