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VEGFA — VIP
Text-mined interactions from Literome
Casibang et al., Lung Cancer 2001
(Carcinoma, Non-Small-Cell Lung...) :
PGE2,
VIP and forskolin
caused increased
VEGF expression in a time- and concentration dependent manner using NSCLC cell line NCI-H157
Collado et al., Regul Pept 2004
(Neovascularization, Pathologic...) :
VIP stimulated
VEGF ( 165 ) protein synthesis as measured by ELISA ...
VIP regulation of
VEGF expression was mediated by VPAC(1) receptor and was cAMP/protein kinase A (PKA) dependent
Collado et al., Biochim Biophys Acta 2005
(Calcium Signaling...) :
As shown by means of real-time RT-PCR,
VIP stimulated
VEGF mRNA expression : the effect was inhibited by 40 % in the presence of curcumin ( an inhibitor of AP-1 binding ), and it was dependent on Ca ( 2+ ) since BAPTA/AM inhibited this VIP action by 43 %
Fernández-MartÃnez et al., Peptides 2009
(Prostatic Neoplasms) :
The regulatory
role of
VIP on cyclooxygenase-2 (COX-2) and
vascular endothelial growth factor ( VEGF ) expression as well as on matrix metalloproteinase-2 and 9 ( MMP-2 and 9 ) activities was examined
Kakurai et al., Br J Dermatol 2009
(Psoriasis) :
In this study, we attempted to determine whether
VIP could
increase the production of
VEGF in human keratinocytes
Yu et al., Neuropeptides 2010
:
In the present study, we examined the
effect and mechanism of
VIP on
vascular endothelial growth factor ( VEGF ) production by HaCaT cells which is a spontaneous, immortalized, human keratinocyte cell line ... However, this increase was abrogated by pretreatment with an extracellular signal regulated kinase ( ERK ) inhibitor PD98059 or p38MAPK inhibitor SB203580 ; pretreatment with c-Jun N-terminal kinase (JNK) inhibitor SP600125 did not attenuate the
effects of
VIP on the expression of
VEGF ... These results suggest that
VIP increases the expression of
VEGF through the ERK1/2 and p38MAPK signaling pathway in human HaCaT cells
Zhao et al., Zhongguo Fei Ai Za Zhi 2006
:
[ c-fos antisense oligodeoxynucleotide reduces
VIP induced upregulation of
VEGF expression in small cell lung cancer cells ] ... The aim of this study is to use c-fos antisense oligodeoxynucleotide ( ASO ) to block c-fos expression and to explore whether c-fos can directly regulate
VIP induced
VEGF expression in small cell lung cancer ( SCLC ) cells ... c-fos ASO significantly reversed
VIP induced upregulation of
VEGF mRNA expression ( P < 0.01 ) ...
VIP can
increase the expression and secretion of
VEGF in lung cancer cells by activating the transcription factor c-fos, then promote the angiogenesis of lung cancer and thus play an important role in the pathogenesis of lung cancer
Yang et al., Peptides 2013
:
The
VIP induced
VEGF production was blocked by H89, a protein kinase A (PKA) inhibitor