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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03918naa a2200517 4500 | |
| 001 | oai:DiVA.org:uu-400532 | |
| 003 | SwePub | |
| 008 | 191223s2019 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4005322 URI |
| 024 | 7 | a https://doi.org/10.3390/cells81216452 DOI |
| 040 | a (SwePub)uu | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Pietilä, Ilkkau Uppsala universitet,Institutionen för medicinsk cellbiologi,Vaskulärbiologi4 aut0 (Swepub:uu)ilkpi999 |
| 245 | 1 0 | a Temporal Dynamics of VEGFA-Induced VEGFR2/FAK Co-Localization Depend on SHB |
| 264 | c 2019-12-15 | |
| 264 | 1 | a Basel, Switzerland :b MDPI,c 2019 |
| 338 | a electronic2 rdacarrier | |
| 520 | a Focal adhesion kinase (FAK) is essential for vascular endothelial growth factor-A (VEGFA)/VEGF receptor-2 (VEGFR2)-stimulated angiogenesis and vascular permeability. We have previously noted that presence of the Src homology-2 domain adapter protein B (SHB) is of relevance for VEGFA-stimulated angiogenesis in a FAK-dependent manner. The current study was conducted in order address the temporal dynamics of co-localization between these components in HEK293 and primary lung endothelial cells (EC) by total internal reflection fluorescence microscopy (TIRF). An early (<2.5 min) VEGFA-induced increase in VEGFR2 co-localization with SHB was dependent on tyrosine 1175 in VEGFR2. VEGFA also enhanced SHB co-localization with FAK. FAK co-localization with VEGFR2 was dependent on SHB since it was significantly lower in SHB deficient EC after VEGFA addition. Absence of SHB also resulted in a gradual decline of VEGFR2 co-localization with FAK under basal (prior to VEGFA addition) conditions. A similar basal response was observed with expression of the Y1175F-VEGFR2 mutant in wild type EC. The distribution of focal adhesions in SHB-deficient EC was altered with a primarily perinuclear location. These live cell data implicate SHB as a key component regulating FAK activity in response to VEGFA/VEGFR2. | |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaper0 (SwePub)3012 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Basic Medicine0 (SwePub)3012 hsv//eng |
| 650 | 7 | a NATURVETENSKAPx Biologix Cellbiologi0 (SwePub)106042 hsv//swe |
| 650 | 7 | a NATURAL SCIENCESx Biological Sciencesx Cell Biology0 (SwePub)106042 hsv//eng |
| 653 | a VEGFR2 | |
| 653 | a FAK | |
| 653 | a SHB | |
| 653 | a TIRF | |
| 653 | a focal adhesions | |
| 653 | a angiogenesis | |
| 653 | a Molekylär cellbiologi | |
| 653 | a Molecular Cellbiology | |
| 700 | 1 | a van Mourik, Djenolanu Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut |
| 700 | 1 | a Tamelander, Andreasu Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut |
| 700 | 1 | a Kriz, Vitezslavu Institute of Molecular Genetics of the CAS, 14220 Prague, Czech Republic4 aut |
| 700 | 1 | a Claesson-Welsh, Lenau Uppsala universitet,Institutionen för immunologi, genetik och patologi4 aut0 (Swepub:uu)lcl04207 |
| 700 | 1 | a Tengholm, Anders,d 1971-u Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut0 (Swepub:uu)andeteng |
| 700 | 1 | a Welsh, Michael,d 1957-u Uppsala universitet,Institutionen för medicinsk cellbiologi4 aut0 (Swepub:uu)michwels |
| 710 | 2 | a Uppsala universitetb Institutionen för medicinsk cellbiologi4 org |
| 773 | 0 | t Cellsd Basel, Switzerland : MDPIg 8:12q 8:12x 2073-4409 |
| 856 | 4 | u https://doi.org/10.3390/cells8121645y Fulltext |
| 856 | 4 | u https://uu.diva-portal.org/smash/get/diva2:1381576/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print |
| 856 | 4 | u https://www.mdpi.com/2073-4409/8/12/1645/pdf |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-400532 |
| 856 | 4 8 | u https://doi.org/10.3390/cells8121645 |
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