TEK tirozinska kinaza

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TEK tirozinska kinaza, endotelna

PDB prikaz baziran na 1fvr.
Dostupne strukture
1FVR, 2GY5, 2GY7, 2OO8, 2OSC, 2P4I, 2WQB, 3BEA, 3L8P, 4K0V
Identifikatori
SimboliTEK; CD202B; TIE-2; TIE2; VMCM; VMCM1
Vanjski IDOMIM: 600221 MGI: 98664 HomoloGene: 397 GeneCards: TEK Gene
EC broj2.7.10.1
Ontologija gena
Molekulska funkcija aktivnost proteinske kinaze
aktivnost proteinske tirozinske kinaze
aktivnost transmembranske receptorske proteinske tirozinske kinaze
Ćelijska komponenta ekstracelularni region
citoplazma
aktinski filament
Biološki proces angiogeneza
respons na hipoksiju
pozitivna regulacija proteinske fosforilacije
Pregled RNK izražavanja
podaci
Ortolozi
VrstaČovekMiš
Entrez701021687
EnsemblENSG00000120156ENSMUSG00000006386
UniProtQ02763Q02858
Ref. Sekv. (iRNK)NM_000459NM_001290549
Ref. Sekv. (protein)NP_000450NP_001277478
Lokacija (UCSC)Chr 9:
27.11 - 27.23 Mb
Chr 4:
94.74 - 94.87 Mb
PubMed pretraga[1][2]

Receptor angiopoietina 1 je protein koji je kod ljudi kodiran TEK genom.[1][2] TEK se takođe označava sa CD202B (klaster diferencijacije 202B).

TEK receptorska tirozinska kinaza je izražena skoro isključivo u endotelnim ćelijama kod miševa, pacova, i ljudi. Ovaj receptor poseduje jedinstveni ekstracelularni domen koji sadrži 2 imunoglobulinu slične petlje razdvojene sa 3 ponavljanja slična epidermalnom faktoru rasta koja su povezana sa 3 ponavljanja slična fibronektinu tipa III. Ligand ovog receptora je angiopoietin-1. Defekti u TEK su asocirani sa naslednim venskim malformacijama; TEK signalni put je kritičan za komunikaciju endotelnih ćelija i glatkih mišičnih ćelija tokom venske morfogeneze. TEK je blisko srodan sa TIE receptorskom tirozinskom kinazom.[3]

Interakcije

TEK tirozinska kinaza formira interakcije sa DOK2,[4][5] Angiopoietin 1[6][7][8][9] i ANGPT2.[6][8][9]

Reference

  1. Partanen J, Armstrong E, Makela TP, Korhonen J, Sandberg M, Renkonen R, Knuutila S, Huebner K, Alitalo K (April 1992). „A novel endothelial cell surface receptor tyrosine kinase with extracellular epidermal growth factor homology domains”. Mol Cell Biol 12 (4): 1698–707. PMC 369613. PMID 1312667. 
  2. Boon LM, Mulliken JB, Vikkula M, Watkins H, Seidman J, Olsen BR, Warman ML (February 1995). „Assignment of a locus for dominantly inherited venous malformations to chromosome 9p”. Hum Mol Genet 3 (9): 1583–7. DOI:10.1093/hmg/3.9.1583. PMID 7833915. 
  3. „Entrez Gene: TEK TEK tyrosine kinase, endothelial (venous malformations, multiple cutaneous and mucosal)”. 
  4. Jones, N; Dumont D J (September 1998). „The Tek/Tie2 receptor signals through a novel Dok-related docking protein, Dok-R”. Oncogene (ENGLAND) 17 (9): 1097–108. DOI:10.1038/sj.onc.1202115. ISSN 0950-9232. PMID 9764820. 
  5. Master, Z; Jones N; Tran J; Jones J; Kerbel R S; Dumont D J (November 2001). „Dok-R plays a pivotal role in angiopoietin-1-dependent cell migration through recruitment and activation of Pak”. EMBO J. (England) 20 (21): 5919–28. DOI:10.1093/emboj/20.21.5919. ISSN 0261-4189. PMC 125712. PMID 11689432. 
  6. 6,0 6,1 Fiedler, Ulrike; Krissl Tanja, Koidl Stefanie, Weiss Cornelia, Koblizek Thomas, Deutsch Urban, Martiny-Baron Georg, Marmé Dieter, Augustin Hellmut G (January 2003). „Angiopoietin-1 and angiopoietin-2 share the same binding domains in the Tie-2 receptor involving the first Ig-like loop and the epidermal growth factor-like repeats”. J. Biol. Chem. (United States) 278 (3): 1721–7. DOI:10.1074/jbc.M208550200. ISSN 0021-9258. PMID 12427764. 
  7. Davis, S; Aldrich T H, Jones P F, Acheson A, Compton D L, Jain V, Ryan T E, Bruno J, Radziejewski C, Maisonpierre P C, Yancopoulos G D (December 1996). „Isolation of angiopoietin-1, a ligand for the TIE2 receptor, by secretion-trap expression cloning”. Cell (UNITED STATES) 87 (7): 1161–9. DOI:10.1016/S0092-8674(00)81812-7. ISSN 0092-8674. PMID 8980223. 
  8. 8,0 8,1 Sato, A; Iwama A; Takakura N; Nishio H; Yancopoulos G D; Suda T (August 1998). „Characterization of TEK receptor tyrosine kinase and its ligands, Angiopoietins, in human hematopoietic progenitor cells”. Int. Immunol. (ENGLAND) 10 (8): 1217–27. DOI:10.1093/intimm/10.8.1217. ISSN 0953-8178. PMID 9723709. 
  9. 9,0 9,1 Maisonpierre, P C; Suri C, Jones P F, Bartunkova S, Wiegand S J, Radziejewski C, Compton D, McClain J, Aldrich T H, Papadopoulos N, Daly T J, Davis S, Sato T N, Yancopoulos G D (July 1997). „Angiopoietin-2, a natural antagonist for Tie2 that disrupts in vivo angiogenesis”. Science (UNITED STATES) 277 (5322): 55–60. DOI:10.1126/science.277.5322.55. ISSN 0036-8075. PMID 9204896. 

Literatura

  • Huang L, Turck CW, Rao P, Peters KG (1995). „GRB2 and SH-PTP2: potentially important endothelial signaling molecules downstream of the TEK/TIE2 receptor tyrosine kinase.”. Oncogene 11 (10): 2097–103. PMID 7478529. 
  • Deans JP, Kalt L, Ledbetter JA, et al. (1995). „Association of 75/80-kDa phosphoproteins and the tyrosine kinases Lyn, Fyn, and Lck with the B cell molecule CD20. Evidence against involvement of the cytoplasmic regions of CD20.”. J. Biol. Chem. 270 (38): 22632–8. DOI:10.1074/jbc.270.38.22632. PMID 7545683. 
  • Gallione CJ, Pasyk KA, Boon LM, et al. (1995). „A gene for familial venous malformations maps to chromosome 9p in a second large kindred.”. J. Med. Genet. 32 (3): 197–9. DOI:10.1136/jmg.32.3.197. PMC 1050316. PMID 7783168. 
  • Robertson NG, Khetarpal U, Gutiérrez-Espeleta GA, et al. (1995). „Isolation of novel and known genes from a human fetal cochlear cDNA library using subtractive hybridization and differential screening.”. Genomics 23 (1): 42–50. DOI:10.1006/geno.1994.1457. PMID 7829101. 
  • Dumont DJ, Anderson L, Breitman ML, Duncan AM (1995). „Assignment of the endothelial-specific protein receptor tyrosine kinase gene (TEK) to human chromosome 9p21.”. Genomics 23 (2): 512–3. DOI:10.1006/geno.1994.1536. PMID 7835909. 
  • Ziegler SF, Bird TA, Schneringer JA, et al. (1993). „Molecular cloning and characterization of a novel receptor protein tyrosine kinase from human placenta.”. Oncogene 8 (3): 663–70. PMID 8382358. 
  • Davis S, Aldrich TH, Jones PF, et al. (1997). „Isolation of angiopoietin-1, a ligand for the TIE2 receptor, by secretion-trap expression cloning.”. Cell 87 (7): 1161–9. DOI:10.1016/S0092-8674(00)81812-7. PMID 8980223. 
  • Suri C, Jones PF, Patan S, et al. (1997). „Requisite role of angiopoietin-1, a ligand for the TIE2 receptor, during embryonic angiogenesis.”. Cell 87 (7): 1171–80. DOI:10.1016/S0092-8674(00)81813-9. PMID 8980224. 
  • Vikkula M, Boon LM, Carraway KL, et al. (1997). „Vascular dysmorphogenesis caused by an activating mutation in the receptor tyrosine kinase TIE2.”. Cell 87 (7): 1181–90. DOI:10.1016/S0092-8674(00)81814-0. PMID 8980225. 
  • Witzenbichler B, Maisonpierre PC, Jones P, et al. (1998). „Chemotactic properties of angiopoietin-1 and -2, ligands for the endothelial-specific receptor tyrosine kinase Tie2.”. J. Biol. Chem. 273 (29): 18514–21. DOI:10.1074/jbc.273.29.18514. PMID 9660821. 
  • Asahara T, Chen D, Takahashi T, et al. (1998). „Tie2 receptor ligands, angiopoietin-1 and angiopoietin-2, modulate VEGF-induced postnatal neovascularization.”. Circ. Res. 83 (3): 233–40. DOI:10.1161/01.res.83.3.233. PMID 9710115. 
  • Sato A, Iwama A, Takakura N, et al. (1998). „Characterization of TEK receptor tyrosine kinase and its ligands, Angiopoietins, in human hematopoietic progenitor cells.”. Int. Immunol. 10 (8): 1217–27. DOI:10.1093/intimm/10.8.1217. PMID 9723709. 
  • Jones N, Dumont DJ (1998). „The Tek/Tie2 receptor signals through a novel Dok-related docking protein, Dok-R.”. Oncogene 17 (9): 1097–108. DOI:10.1038/sj.onc.1202115. PMID 9764820. 
  • De Sepulveda P, Okkenhaug K, Rose JL, et al. (1999). „Socs1 binds to multiple signalling proteins and suppresses steel factor-dependent proliferation.”. EMBO J. 18 (4): 904–15. DOI:10.1093/emboj/18.4.904. PMC 1171183. PMID 10022833. 
  • Valenzuela DM, Griffiths JA, Rojas J, et al. (1999). „Angiopoietins 3 and 4: diverging gene counterparts in mice and humans.”. Proc. Natl. Acad. Sci. U.S.A. 96 (5): 1904–9. DOI:10.1073/pnas.96.5.1904. PMC 26709. PMID 10051567. 
  • Calvert JT, Riney TJ, Kontos CD, et al. (1999). „Allelic and locus heterogeneity in inherited venous malformations.”. Hum. Mol. Genet. 8 (7): 1279–89. DOI:10.1093/hmg/8.7.1279. PMID 10369874. 
  • Jones N, Master Z, Jones J, et al. (1999). „Identification of Tek/Tie2 binding partners. Binding to a multifunctional docking site mediates cell survival and migration.”. J. Biol. Chem. 274 (43): 30896–905. DOI:10.1074/jbc.274.43.30896. PMID 10521483. 
  • Fachinger G, Deutsch U, Risau W (1999). „Functional interaction of vascular endothelial-protein-tyrosine phosphatase with the angiopoietin receptor Tie-2.”. Oncogene 18 (43): 5948–53. DOI:10.1038/sj.onc.1202992. PMID 10557082. 

Vanjske veze

  • GeneReviews/NCBI/NIH/UW entry on Multiple Cutaneous and Mucosal Venous Malformations
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PDB Galerija
1fvr: TIE2 kinazni domen
1fvr: TIE2 kinazni domen  
2gy5: Kristalna struktura Tie2 domena vezivanja liganda
2gy5: Kristalna struktura Tie2 domena vezivanja liganda  
2gy7: Kristalna struktura angiopoietin-2/Tie2 kompleksa
2gy7: Kristalna struktura angiopoietin-2/Tie2 kompleksa  
2oo8: Sinteza, strukturna analiza, i SAR studije triazinskih derivata kao potentnih, selektivnih Tie-2 inhibitora
2oo8: Sinteza, strukturna analiza, i SAR studije triazinskih derivata kao potentnih, selektivnih Tie-2 inhibitora  
2osc: Sinteza, strukturna analiza, i SAR studije triazinskih derivata kao potentnih, selektivnih Tie-2 inhibitora
2osc: Sinteza, strukturna analiza, i SAR studije triazinskih derivata kao potentnih, selektivnih Tie-2 inhibitora  
2p4i: Evolucija visoko selektivnih i potentnih 2-(piridin-2-il)-1,3,5-triazin Tie-2 kinaznih inhibitora
2p4i: Evolucija visoko selektivnih i potentnih 2-(piridin-2-il)-1,3,5-triazin Tie-2 kinaznih inhibitora  
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Receptori faktora rasta
EGFR • ERBB2 • ERBB3 • ERBB4
IGF1R • INSR • INSRR
CSF1R • FLT3 • KIT • PDGFR (PDGFRA, PDGFRB)
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LTK receptorska familija
LTK • ALK
TIE receptorska familija
TIE • TEK
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ROR1 • ROR2
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DDR1 • DDR2
PTK7 receptorska familija
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ROS1
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1-50
CD1 (a-c, 1A, 1D, 1E) • CD2 • CD3 (γ, δ, ε) • CD4 • CD5 • CD6 • CD7 • CD8 (a) • CD9 • CD10 • CD11 (a, b, c) • CD13 • CD14 • CD15 • CD16 (A, B) • CD18 • CD19 • CD20 • CD21 • CD22 • CD23 • CD24 • CD25 • CD26 • CD27 • CD28 • CD29 • CD30 • CD31 • CD32 (A, B) • CD33 • CD34 • CD35 • CD36 • CD37 • CD38 • CD39 • CD40 • CD41 • CD42 (a, b, c, d) • CD43 • CD44 • CD45 • CD46 • CD47 • CD48 • CD49 (a, b, c, d, e, f) • CD50
51-100
CD51 • CD52 • CD53 • CD54 • CD55 • CD56 • CD57 • CD58 • CD59 • CD61 • CD62 (E, L, P) • CD63 • CD64 (A, B, C) • CD66 (a, b, c, d, e, f) • CD68 • CD69 • CD70 • CD71 • CD72 • CD73 • CD74 • CD78 • CD79 (a, b) • CD80 • CD81 • CD82 • CD83 • CD84 • CD85 (a, d, e, h, j, k) • CD86 • CD87 • CD88 • CD89 • CD90 • CD91- CD92 • CD93 • CD94 • CD95 • CD96 • CD97 • CD98 • CD99 • CD100
101-150
CD101 • CD102 • CD103 • CD104 • CD105 • CD106 • CD107 (a, b) • CD108 • CD109 • CD110 • CD111 • CD112 • CD113 • CD114 • CD115 • CD116 • CD117 • CD118 • CD119 • CD120 (a, b) • CD121 (a, b) • CD122 • CD123 • CD124 • CD125 • CD126 • CD127 • CD129 • CD130 • CD131 • CD132 • CD133 • CD134 • CD135 • CD136 • CD137 • CD138 • CD140b • CD141 • CD142 • CD143 • CD144 • CD146 • CD147 • CD148 • CD150
151-200
CD151 • CD152 • CD153 • CD154 • CD155 • CD156 (a, b, c) • CD157 • CD158 (a, d, e, i, k) • CD159 (a, c) • CD160 • CD161 • CD162 • CD163 • CD164 • CD166 • CD167 (a, b) • CD168 • CD169 • CD170 • CD171 • CD172 (a, b, g) • CD174 • CD177 • CD178 • CD179 (a, b) • CD181 • CD182 • CD183 • CD184 • CD185 • CD186 • CD191 • CD192 • CD193 • CD194 • CD195 • CD196 • CD197 • CDw198 • CDw199 • CD200
201-250
CD201 • CD202b • CD204 • CD205 • CD206 • CD207 • CD208 • CD209 • CDw210 (a, b) • CD212 • CD213a (1, 2) • CD217 • CD218 (a, b) • CD220 • CD221 • CD222 • CD223 • CD224 • CD225 • CD226 • CD227 • CD228 • CD229 • CD230 • CD233 • CD234 • CD235 (a, b) • CD236 • CD238 • CD239 • CD240CE • CD241 • CD243 • CD244 • CD246 • CD247- CD248 • CD249
251-300
CD252 • CD253 • CD254 • CD256 • CD257 • CD258 • CD261 • CD262 • CD264 • CD265 • CD266 • CD267 • CD268 • CD269 • CD271 • CD272 • CD273 • CD274 • CD275 • CD276 • CD278 • CD279 • CD280 • CD281 • CD282 • CD283 • CD284 • CD286 • CD288 • CD289 • CD290 • CD292 • CDw293 • CD294 • CD295 • CD297 • CD298 • CD299
301-350
CD300A • CD301 • CD302 • CD303 • CD304 • CD305 • CD306 • CD307 • CD309 • CD312 • CD314 • CD315 • CD316 • CD317 • CD318 • CD320 • CD321 • CD322 • CD324 • CD325 • CD326 • CD328 • CD329 • CD331 • CD332 • CD333 • CD334 • CD335 • CD336 • CD337 • CD338 • CD339 • CD340 • CD344 • CD349 • CD350