Gene interactions and pathways from curated databases and text-mining

◀ Back to VEGFA

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-Martínez 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