HCSGD entry for FLT1
1. General information
| Official gene symbol | FLT1 |
|---|---|
| Entrez ID | 2321 |
| Gene full name | fms-related tyrosine kinase 1 |
| Other gene symbols | FLT FLT-1 VEGFR-1 VEGFR1 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0001569 | Patterning of blood vessels | IEA | biological_process |
| GO:0002040 | Sprouting angiogenesis | IEA | biological_process |
| GO:0002548 | Monocyte chemotaxis | IDA | biological_process |
| GO:0004714 | Transmembrane receptor protein tyrosine kinase activity | TAS | molecular_function |
| GO:0005021 | Vascular endothelial growth factor-activated receptor activity | IDA IMP | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005524 | ATP binding | IEA | molecular_function |
| GO:0005615 | Extracellular space | TAS | cellular_component |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005730 | Nucleolus | IDA | cellular_component |
| GO:0005737 | Cytoplasm | IDA | cellular_component |
| GO:0005768 | Endosome | IEA | cellular_component |
| GO:0005794 | Golgi apparatus | IDA | cellular_component |
| GO:0005886 | Plasma membrane | IDA TAS | cellular_component |
| GO:0005887 | Integral component of plasma membrane | IDA | cellular_component |
| GO:0007169 | Transmembrane receptor protein tyrosine kinase signaling pathway | TAS | biological_process |
| GO:0008284 | Positive regulation of cell proliferation | TAS | biological_process |
| GO:0010863 | Positive regulation of phospholipase C activity | IMP | biological_process |
| GO:0014068 | Positive regulation of phosphatidylinositol 3-kinase signaling | IMP | biological_process |
| GO:0016477 | Cell migration | IMP | biological_process |
| GO:0018108 | Peptidyl-tyrosine phosphorylation | IDA | biological_process |
| GO:0019838 | Growth factor binding | IPI | molecular_function |
| GO:0030154 | Cell differentiation | IEA | biological_process |
| GO:0030335 | Positive regulation of cell migration | IDA | biological_process |
| GO:0030949 | Positive regulation of vascular endothelial growth factor receptor signaling pathway | IDA | biological_process |
| GO:0035924 | Cellular response to vascular endothelial growth factor stimulus | IDA | biological_process |
| GO:0036323 | Vascular endothelial growth factor receptor-1 signaling pathway | IDA | biological_process |
| GO:0036326 | VEGF-A-activated receptor activity | IDA | molecular_function |
| GO:0036327 | VEGF-B-activated receptor activity | IDA | molecular_function |
| GO:0036332 | Placental growth factor-activated receptor activity | IDA | molecular_function |
| GO:0042802 | Identical protein binding | IEA | molecular_function |
| GO:0043235 | Receptor complex | IDA | cellular_component |
| GO:0043406 | Positive regulation of MAP kinase activity | IDA | biological_process |
| GO:0043410 | Positive regulation of MAPK cascade | IDA | biological_process |
| GO:0043552 | Positive regulation of phosphatidylinositol 3-kinase activity | IMP | biological_process |
| GO:0045766 | Positive regulation of angiogenesis | IMP | biological_process |
| GO:0046777 | Protein autophosphorylation | IDA | biological_process |
| GO:0048010 | Vascular endothelial growth factor receptor signaling pathway | IDA IMP TAS | biological_process |
| GO:0048514 | Blood vessel morphogenesis | ISS | biological_process |
| GO:0048598 | Embryonic morphogenesis | ISS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.2634962159 | 0.2860913301 | 0.9578770197 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Up | 0.0115575222 |
| GSE13712_SHEAR | Up | 0.0969424256 |
| GSE13712_STATIC | Down | -0.1963589571 |
| GSE19018 | Down | -0.8662967811 |
| GSE19899_A1 | Up | 0.3072471413 |
| GSE19899_A2 | Up | 0.6231228167 |
| PubMed_21979375_A1 | Down | -1.2100654599 |
| PubMed_21979375_A2 | Up | 0.0958210268 |
| GSE35957 | Up | 0.0236291465 |
| GSE36640 | Up | 0.4959374265 |
| GSE54402 | Up | 1.3071563543 |
| GSE9593 | Up | 0.0024067744 |
| GSE43922 | Up | 0.0493768833 |
| GSE24585 | Down | -0.4713209232 |
| GSE37065 | Down | -0.0953728236 |
| GSE28863_A1 | Down | -0.0643007612 |
| GSE28863_A2 | Down | -0.1989193815 |
| GSE28863_A3 | Up | 0.0830789030 |
| GSE28863_A4 | Up | 0.0692214591 |
| GSE48662 | Up | 0.0305114722 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Sorafenib | DB00398 | APRD01304 | DB07438 |
| Sunitinib | DB01268 | DB07417 |
| Vatalanib | DB04879 | - |
| TG100801 | DB05075 | - |
| OSI-930 | DB05913 | - |
| ABT-869 | DB06080 | - |
| IMC-1C11 | DB06101 | - |
| Pazopanib | DB06589 | - |
| Axitinib | DB06626 | - |
| N-(4-chlorophenyl)-2-[(pyridin-4-ylmethyl)amino]benzamide | DB07288 | - |
| Regorafenib | DB08896 | - |
| Lenvatinib | DB09078 | - |
| Nintedanib | DB09079 | - |
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-200b-3p | MIMAT0000318 | MIRT006441 | Luciferase reporter assay//Western blot | Functional MTI | 21544626 |
| hsa-miR-100-5p | MIMAT0000098 | MIRT006850 | Luciferase reporter assay | Functional MTI | 22955733 |
| hsa-miR-200c-3p | MIMAT0000617 | MIRT006885 | Luciferase reporter assay//Western blot | Functional MTI | 22569286 |
| hsa-miR-155-5p | MIMAT0000646 | MIRT020776 | qRT-PCR | Functional MTI (Weak) | 21310411 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 3 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 21622994 | RESULTS: Uremic MSCs showed decreased expression of vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)1 and stromal cell-derived factor (SDF)-1alpha, increased cellular senescence, decreased proliferation, defects in migration in response to VEGF and SDF-1alpha and in vitro tube formation |
| 21622994 | Uremia decreased hypoxia-inducible factor-1alpha, VEGF and VEGFR1 expression under hypoxia and Akt phosphorylation in both basal and VEGF-stimulated states |
| 20027224 | Interestingly, genes that showed the most significant link include those that mediate various signaling pathways implicated in colorectal tumorigenesis, such as BMP3 and BMP6 (BMP signaling), EPHA3, KIT, and FLT1 (receptor tyrosine kinases) and SMO (Hedgehog signaling) |
| 18583712 | Vascular endothelial growth factor (VEGF) binds both VEGF receptor-1 (VEGFR-1) and VEGF receptor-2 (VEGFR-2) |
| 18583712 | Recently, specific ligands for VEGFR-1 have been reported to have beneficial effects when used to treat ischemic diseases |
| 18583712 | However, the role of VEGFR-1 in angiogenesis is not fully understood |
| 18583712 | In this study, we showed that VEGFR-1 performs "fine tuning" of VEGF signaling to induce neovascularization |
| 18583712 | We examined the effects of retroviral vectors expressing a small interference RNA that targeted either the VEGFR-1 gene or the VEGFR-2 gene |
| 18583712 | Deletion of either VEGFR-1 or VEGFR-2 reduced the ability of endothelial cells to form capillaries |
| 18583712 | Deletion of VEGFR-1 markedly reduced endothelial cell proliferation and induced premature senescence of endothelial cells |
| 18583712 | When VEGFR-1 expression was blocked, VEGF constitutively activated Akt signals and thus induced endothelial cell senescence via a p53-dependent pathway |
| 18583712 | VEGFR-1(+/-) mice exhibited an increase of endothelial Akt activity and showed an impaired neovascularization in response to ischemia, and this impairment was ameliorated in VEGFR-1(+/-) Akt1(+/-) mice |
| 18583712 | These results suggest that VEGFR-1 plays a critical role in the maintenance of endothelial integrity by modulating the VEGF/Akt signaling pathway |
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