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Temporal Dynamics o...
Temporal Dynamics of VEGFA-Induced VEGFR2/FAK Co-Localization Depend on SHB
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- Pietilä, Ilkka (författare)
- Uppsala universitet,Institutionen för medicinsk cellbiologi,Vaskulärbiologi
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- van Mourik, Djenolan (författare)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Tamelander, Andreas (författare)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Kriz, Vitezslav (författare)
- Institute of Molecular Genetics of the CAS, 14220 Prague, Czech Republic
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- Claesson-Welsh, Lena (författare)
- Uppsala universitet,Institutionen för immunologi, genetik och patologi
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- Tengholm, Anders, 1971- (författare)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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- Welsh, Michael, 1957- (författare)
- Uppsala universitet,Institutionen för medicinsk cellbiologi
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(creator_code:org_t)
- 2019-12-15
- 2019
- Engelska.
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Ingår i: Cells. - Basel, Switzerland : MDPI. - 2073-4409. ; 8:12
- Relaterad länk:
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https://doi.org/10.3...
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https://uu.diva-port... (primary) (Raw object)
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https://www.mdpi.com...
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https://urn.kb.se/re...
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https://doi.org/10.3...
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Abstract
Ämnesord
Stäng
- 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.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine (hsv//eng)
- NATURVETENSKAP -- Biologi -- Cellbiologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Cell Biology (hsv//eng)
Nyckelord
- VEGFR2
- FAK
- SHB
- TIRF
- focal adhesions
- angiogenesis
- Molekylär cellbiologi
- Molecular Cellbiology
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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