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Gene Information
Gene symbol: KDR
Gene name: kinase insert domain receptor (a type III receptor tyrosine kinase)
HGNC ID: 6307
Synonyms: FLK1, VEGFR, VEGFR2, CD309
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | NPHS1 | 1 hits |
| 2 | NPTX1 | 1 hits |
| 3 | NPTX2 | 1 hits |
| 4 | VEGFA | 1 hits |
| 5 | VEGFC | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 22038228 | The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases. |
| 2 | 22038228 | VEGF-C over-expression in these cases was followed by downregulation of VEGFR-2. |
| 3 | 16239266 | The VEGF-induced elevation of LpA/Vi was blocked by the selective VEGF-R2 inhibitor ZM323881. |
| 4 | 16436677 | Additionally, VEGFR2 was constitutively phosphorylated in the liver, lung, adipose, and kidney in vivo, providing evidence consistent with a role for VEGF in adult tissues. |
| 5 | 20688931 | Unlike cell culture models, enhanced expression of VEGF by podocytes in vivo caused foot process fusion and alterations in slit diaphragm-associated proteins; however, inhibition of VEGFR-2 could not rescue this defect. |
| 6 | 12620928 | Normal human podocytes are also known to express neuropilin-1, VEGF, and are VEGF-R2 negative. |
| 7 | 16597608 | Differentiated podocytes expressed eightfold higher VEGFR2 mRNA levels than undifferentiated podocytes, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels were similar. |
| 8 | 16597608 | VEGF(165) induced a twofold increase in VEGFR2 mRNA and protein levels, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels remained unchanged. |
| 9 | 16597608 | VEGF(165) induced VEGFR2 phosphorylation. |
| 10 | 19828679 | We demonstrated that ablation of VEGF-A or VEGF-C as well as treatment with bevacizumab or a VEGFR-2/-3 tyrosine kinase inhibitor led to reduced podocyte survival. |
| 11 | 21937443 | We previously showed that in vivo nephrin associates with VEGF receptor-2 (VEGFR2), the signaling receptor for VEGF-A. |