FLT4;VEGFR3

Vascular endothelial growth factor receptor 3 (VEGFR-3) (EC 2.7.10.1) (Fms-like tyrosine kinase 4) (FLT-4) (Tyrosine-protein kinase receptor FLT4)

Homo sapiens (Human)

152757

1363

Pending Verification

Vascular endothelial growth factor receptor 3 (VEGFR-3) (EC 2.7.10.1) (Fms-like tyrosine kinase 4) (FLT-4) (Tyrosine-protein kinase receptor FLT4)

Lymphedema, hereditary, 1A (LMPH1A) [MIM:153100]: A chronic disabling condition which results in swelling of the extremities due to altered lymphatic flow. Patients with lymphedema suffer from recurrent local infections and physical impairment. {ECO:0000269|PubMed:10835628, ECO:0000269|PubMed:10856194, ECO:0000269|PubMed:12881528, ECO:0000269|PubMed:15102829, ECO:0000269|PubMed:16924388, ECO:0000269|PubMed:16965327, ECO:0000269|PubMed:17458866, ECO:0000269|PubMed:19289394, ECO:0000269|PubMed:26091405, ECO:0000269|PubMed:9817924}. Note=The disease is caused by mutations affecting the gene represented in this entry.; Hemangioma, capillary infantile (HCI) [MIM:602089]: A condition characterized by dull red, firm, dome-shaped hemangiomas, sharply demarcated from surrounding skin, usually presenting at birth or occurring within the first two or three months of life. They result from highly proliferative, localized growth of capillary endothelium and generally undergo regression and involution without scarring. {ECO:0000269|PubMed:11807987}. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry.; Note=Plays an important role in tumor lymphangiogenesis, in cancer cell survival, migration, and formation of metastases.

MUTAGEN 446 446 T->E: Decreases autophosphorylation on tyrosine residues upon ligand binding; when associated with A-516. Abolishes autophosphorylation on tyrosine residues upon ligand binding; when associated with A-516 and A-737. {ECO:0000269|PubMed:23878260}.; MUTAGEN 516 516 K->A: Decreases autophosphorylation on tyrosine residues upon ligand binding; when associated with E-446. Abolishes autophosphorylation on tyrosine residues upon ligand binding; when associated with E-446 and A-737. {ECO:0000269|PubMed:23878260}.; MUTAGEN 737 737 R->A: Decreases autophosphorylation on tyrosine residues upon ligand binding. Abolishes autophosphorylation on tyrosine residues upon ligand binding; when associated with E-446 and A-516. {ECO:0000269|PubMed:23878260}.; MUTAGEN 879 879 K->G: Abolishes enzyme activity. {ECO:0000269|PubMed:12881528}.; MUTAGEN 1063 1063 Y->F: Loss of phosphorylation site. No effect on stimulation of cell proliferation and cell migration. {ECO:0000269|PubMed:16076871, ECO:0000269|PubMed:20431062}.; MUTAGEN 1068 1068 Y->F: Global loss of autophosphorylation. Abolishes stimulation of cell proliferation and cell migration. {ECO:0000269|PubMed:16076871, ECO:0000269|PubMed:20431062}.; MUTAGEN 1230 1230 Y->F: Loss of phosphorylation site. Strongly reduces stimulation of cell proliferation and cell migration. {ECO:0000269|PubMed:12881528, ECO:0000269|PubMed:16076871}.; MUTAGEN 1231 1231 Y->F: Loss of phosphorylation site. Strongly reduces stimulation of cell proliferation and cell migration. {ECO:0000269|PubMed:12881528, ECO:0000269|PubMed:16076871}.; MUTAGEN 1265 1265 Y->F: Loss of phosphorylation site. No effect on stimulation of cell proliferation and cell migration. {ECO:0000269|PubMed:12881528}.; MUTAGEN 1333 1333 Y->F: Loss of phosphorylation site. Reduced autophosphorylation. {ECO:0000269|PubMed:12881528, ECO:0000269|PubMed:7675451}.; MUTAGEN 1337 1337 Y->F: Reduced autophosphorylation. Strongly reduces stimulation of cell proliferation and cell migration. {ECO:0000269|PubMed:12881528, ECO:0000269|PubMed:20431062, ECO:0000269|PubMed:7675451}.; MUTAGEN 1363 1363 Y->F: Loss of phosphorylation site. Slighly reduced autophosphorylation. {ECO:0000269|PubMed:12881528, ECO:0000269|PubMed:7675451}.

MQRGAALCLRLWLCLGLLDGLVSGYSMTPPTLNITEESHVIDTGDSLSISCRGQHPLEWAWPGAQEAPATGDKDSEDTGVVRDCEGTDARPYCKVLLLHEVHANDTGSYVCYYKYIKARIEGTTAASSYVFVRDFEQPFINKPDTLLVNRKDAMWVPCLVSIPGLNVTLRSQSSVLWPDGQEVVWDDRRGMLVSTPLLHDALYLQCETTWGDQDFLSNPFLVHITGNELYDIQLLPRKSLELLVGEKLVLNCTVWAEFNSGVTFDWDYPGKQAERGKWVPERRSQQTHTELSSILTIHNVSQHDLGSYVCKANNGIQRFRESTEVIVHENPFISVEWLKGPILEATAGDELVKLPVKLAAYPPPEFQWYKDGKALSGRHSPHALVLKEVTEASTGTYTLALWNSAAGLRRNISLELVVNVPPQIHEKEASSPSIYSRHSRQALTCTAYGVPLPLSIQWHWRPWTPCKMFAQRSLRRRQQQDLMPQCRDWRAVTTQDAVNPIESLDTWTEFVEGKNKTVSKLVIQNANVSAMYKCVVSNKVGQDERLIYFYVTTIPDGFTIESKPSEELLEGQPVLLSCQADSYKYEHLRWYRLNLSTLHDAHGNPLLLDCKNVHLFATPLAASLEEVAPGARHATLSLSIPRVAPEHEGHYVCEVQDRRSHDKHCHKKYLSVQALEAPRLTQNLTDLLVNVSDSLEMQCLVAGAHAPSIVWYKDERLLEEKSGVDLADSNQKLSIQRVREEDAGRYLCSVCNAKGCVNSSASVAVEGSEDKGSMEIVILVGTGVIAVFFWVLLLLIFCNMRRPAHADIKTGYLSIIMDPGEVPLEEQCEYLSYDASQWEFPRERLHLGRVLGYGAFGKVVEASAFGIHKGSSCDTVAVKMLKEGATASEHRALMSELKILIHIGNHLNVVNLLGACTKPQGPLMVIVEFCKYGNLSNFLRAKRDAFSPCAEKSPEQRGRFRAMVELARLDRRRPGSSDRVLFARFSKTEGGARRASPDQEAEDLWLSPLTMEDLVCYSFQVARGMEFLASRKCIHRDLAARNILLSESDVVKICDFGLARDIYKDPDYVRKGSARLPLKWMAPESIFDKVYTTQSDVWSFGVLLWEIFSLGASPYPGVQINEEFCQRLRDGTRMRAPELATPAIRRIMLNCWSGDPKARPAFSELVEILGDLLQGRGLQEEEEVCMAPRSSQSSEEGSFSQVSTMALHIAQADAEDSPPSLQRHSLAARYYNWVSFPGCLARGAETRGSSRMKTFEEFPMTPTTYKGSVDNQTDSGMVLASEEFEQIESRHRQESGFSCKGPGQNVAVTRAHPDSQGRRRRPERGARGGQVFYNSEYGELSEPSEEDHCSPSARVTFFTDNSY

Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFC and VEGFD, and plays an essential role in adult lymphangiogenesis and in the development of the vascular network and the cardiovascular system during embryonic development. Promotes proliferation, survival and migration of endothelial cells, and regulates angiogenic sprouting. Signaling by activated FLT4 leads to enhanced production of VEGFC, and to a lesser degree VEGFA, thereby creating a positive feedback loop that enhances FLT4 signaling. Modulates KDR signaling by forming heterodimers. The secreted isoform 3 may function as a decoy receptor for VEGFC and/or VEGFD and play an important role as a negative regulator of VEGFC-mediated lymphangiogenesis and angiogenesis. Binding of vascular growth factors to isoform 1 or isoform 2 leads to the activation of several signaling cascades; isoform 2 seems to be less efficient in signal transduction, because it has a truncated C-terminus and therefore lacks several phosphorylation sites. Mediates activation of the MAPK1/ERK2, MAPK3/ERK1 signaling pathway, of MAPK8 and the JUN signaling pathway, and of the AKT1 signaling pathway. Phosphorylates SHC1. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase. Promotes phosphorylation of MAPK8 at 'Thr-183' and 'Tyr-185', and of AKT1 at 'Ser-473'. {ECO:0000269|PubMed:11532940, ECO:0000269|PubMed:15102829, ECO:0000269|PubMed:15474514, ECO:0000269|PubMed:16076871, ECO:0000269|PubMed:16452200, ECO:0000269|PubMed:17210781, ECO:0000269|PubMed:19610651, ECO:0000269|PubMed:19779139, ECO:0000269|PubMed:20224550, ECO:0000269|PubMed:20431062, ECO:0000269|PubMed:20445537, ECO:0000269|PubMed:21273538, ECO:0000269|PubMed:7675451, ECO:0000269|PubMed:8700872, ECO:0000269|PubMed:9435229}.

Alternative sequence (1); Beta strand (6); Chain (1); Cross-link (1); Disulfide bond (33); Domain (11); Glycosylation (3); Helix (4); Motif (1); Mutagenesis (3); Natural variant (7); Region (1); Repeat (6); Sequence conflict (5); Signal peptide (1); Topological domain (2); Transmembrane (1); Turn (3); Abundant in heart and skeletal muscle; also ovary and kidney; not in liver.

Vascular endothelial growth factor receptor 3 (VEGFR-3) (EC 2.7.10.1) (Fms-like tyrosine kinase 4) (FLT-4) (Tyrosine-protein kinase receptor FLT4)

Recombinant

HEK293

Lyophilized

7.4-7.5

Sterile-filtered colorless solution

1mg/ml

Standard

PBS

SDS-PAGE

> 98%

RP-HPLC

-20°C

This bioreagent is stable at 4°C (short-term) and -70°C(long-term). After reconstitution, sample may be stored at 4°C for 2-7 days and below -18°C for future use.

Reconstitute in sterile distilled H2O to no less than 100ug/ml; dilute reconstituted stock further in other aqueous solutions if needed. Please review COA for lot-specific instructions. Final measurements should be determined by the end-user for optimal performance.