C-fos-induced growth factor

C-fos-induced growth factor (FIGF) (or vascular endothelial growth factor D, VEGF-D) is a vascular endothelial growth factor that in humans is encoded by the FIGF gene.^[5]

VEGFD
Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes 2XV7
Identifiers
Aliases	VEGFD, VEGF-D, FIGF, C-fos induced growth factor, c-fos induced growth factor (vascular endothelial growth factor D), vascular endothelial growth factor D
External IDs	OMIM: 300091; MGI: 108037; HomoloGene: 3288; GeneCards: VEGFD; OMA:VEGFD - orthologs
Gene location (Human) Chr. X chromosome (human)[1] Band Xp22.2 Start 15,345,596 bp[1] End 15,384,413 bp[1]
Gene location (Mouse) Chr. X chromosome (mouse)[2] Band X F5|X 76.35 cM Start 163,156,374 bp[2] End 163,185,646 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in right lung apex of heart upper lobe of left lung testicle lactiferous duct lower lobe of lung gastrocnemius muscle muscle of thigh gastric mucosa right adrenal cortex Top expressed in left lung lobe tunica media of zone of aorta umbilical cord stroma of bone marrow right lung lumbar spinal ganglion tunica adventitia of aorta right lung lobe vas deferens calvaria More reference expression data BioGPS More reference expression data
Gene ontology Molecular function protein homodimerization activity platelet-derived growth factor receptor binding chemoattractant activity protein binding vascular endothelial growth factor receptor binding growth factor activity vascular endothelial growth factor receptor 3 binding Cellular component membrane extracellular region platelet alpha granule lumen extracellular space Biological process dopaminergic neuron differentiation cell differentiation positive regulation of mast cell chemotaxis platelet degranulation induction of positive chemotaxis multicellular organism development positive regulation of cell population proliferation cell population proliferation positive regulation of cell division positive chemotaxis angiogenesis response to hypoxia positive regulation of endothelial cell proliferation positive regulation of angiogenesis vascular endothelial growth factor receptor signaling pathway regulation of signaling receptor activity response to bacterium positive regulation of protein phosphorylation sprouting angiogenesis vascular endothelial growth factor signaling pathway Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 2277 14205 Ensembl ENSG00000165197 ENSMUSG00000031380 UniProt O43915 P97946 RefSeq (mRNA) NM_004469 NM_010216 NM_001308489 RefSeq (protein) NP_004460 NP_001295418 NP_034346 Location (UCSC) Chr X: 15.35 – 15.38 Mb Chr X: 163.16 – 163.19 Mb PubMed search [3] [4]
Wikidata
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Function

The protein encoded by this gene is a member of the platelet-derived growth factor/vascular endothelial growth factor (PDGF/VEGF) family and is active in angiogenesis, lymphangiogenesis, and endothelial cell growth. This secreted protein undergoes a complex proteolytic maturation, generating multiple processed forms that bind and activate VEGFR-2 and VEGFR-3 receptors. The structure and function of this protein is similar to those of vascular endothelial growth factor C.^[5]

Tumor metastasis to lymph nodes

Lymph node metastasis is very often associated with several types of human malignancies. Cancer cells’ journey to lymph node takes place largely through lymphatic tunnel located in and around of primary tumor. VEGF-D's interactions with VEGFR-3 predominantly expressed in lymphatic vessels plays a key role in restructuring lymphatic channel and, hence, able to alter its functions related to fluid and cell transport along the conduits. VEGF-D has been established to be over-expressed in both tumor tissues and patients’ serum samples in several types of human cancer. In addition, VEGF-D expression has been implicated with increased incidence of regional lymph node metastasis. In experimental mice study, genetically modified tumor cell that was forced to produce VEGF-D protein have been established to boost up regional lymph nodes metastases.^[6]