• Je něco špatně v tomto záznamu ?

Temporal Dynamics of VEGFA-Induced VEGFR2/FAK Co-Localization Depend on SHB

I. Pietilä, D. Van Mourik, A. Tamelander, V. Kriz, L. Claesson-Welsh, A. Tengholm, M. Welsh,

. 2019 ; 8 (12) : . [pub] 20191215

Jazyk angličtina Země Švýcarsko

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc20025402

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.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc20025402
003      
CZ-PrNML
005      
20201222160158.0
007      
ta
008      
201125s2019 sz f 000 0|eng||
009      
AR
024    7_
$a 10.3390/cells8121645 $2 doi
035    __
$a (PubMed)31847469
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a sz
100    1_
$a Pietilä, Ilkka $u Department of Medical Cell Biology, Uppsala University, Box 571, 75123 Uppsala, Sweden. Present address: Department of Immunology, Genetics and Pathology, Uppsala University, 75108 Uppsala, Sweden.
245    10
$a Temporal Dynamics of VEGFA-Induced VEGFR2/FAK Co-Localization Depend on SHB / $c I. Pietilä, D. Van Mourik, A. Tamelander, V. Kriz, L. Claesson-Welsh, A. Tengholm, M. Welsh,
520    9_
$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    _2
$a adaptorové proteiny signální transdukční $x metabolismus $7 D048868
650    _2
$a zvířata $7 D000818
650    _2
$a pohyb buněk $x fyziologie $7 D002465
650    _2
$a endoteliální buňky $x metabolismus $7 D042783
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a fokální adhezní tyrosinkinasy $x genetika $x metabolismus $7 D051416
650    _2
$a HEK293 buňky $7 D057809
650    _2
$a lidé $7 D006801
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a myši $7 D051379
650    _2
$a myši inbrední BALB C $7 D008807
650    _2
$a myši knockoutované $7 D018345
650    _2
$a fyziologická neovaskularizace $x fyziologie $7 D018919
650    _2
$a protoonkogenní proteiny $x metabolismus $7 D011518
650    _2
$a vaskulární endoteliální růstový faktor A $x genetika $x metabolismus $7 D042461
650    _2
$a receptor 2 pro vaskulární endoteliální růstový faktor $x metabolismus $7 D040301
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Van Mourik, Djenolan $u Department of Medical Cell Biology, Uppsala University, Box 571, 75123 Uppsala, Sweden.
700    1_
$a Tamelander, Andreas $u Department of Medical Cell Biology, Uppsala University, Box 571, 75123 Uppsala, Sweden.
700    1_
$a Kriz, Vitezslav $u Institute of Molecular Genetics of the CAS, 14220 Prague, Czech Republic.
700    1_
$a Claesson-Welsh, Lena $u Department of Immunology, Genetics and Pathology, Uppsala University, 75108 Uppsala, Sweden.
700    1_
$a Tengholm, Anders $u Department of Medical Cell Biology, Uppsala University, Box 571, 75123 Uppsala, Sweden.
700    1_
$a Welsh, Michael $u Department of Medical Cell Biology, Uppsala University, Box 571, 75123 Uppsala, Sweden.
773    0_
$w MED00194911 $t Cells $x 2073-4409 $g Roč. 8, č. 12 (2019)
856    41
$u https://pubmed.ncbi.nlm.nih.gov/31847469 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20201125 $b ABA008
991    __
$a 20201222160154 $b ABA008
999    __
$a ok $b bmc $g 1599547 $s 1116088
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2019 $b 8 $c 12 $e 20191215 $i 2073-4409 $m Cells $n Cells $x MED00194911
LZP    __
$a Pubmed-20201125

Najít záznam

Citační ukazatele

Možnosti archivace