FGFR3

FGFR3
Dostupne strukture
PDB	Pretraga ortologa: PDBe RCSB
Spisak PDB ID kodova
	1RY7, 2LZL, 4K33
Identifikatori
Aliasi	FGFR3
Vanjski ID-jevi	OMIM: 134934 MGI: 95524 HomoloGene: 55437 GeneCards: FGFR3
Lokacija gena (čovjek)
Hrom.	Hromosom 4 (čovjek)
Kraj	1,808,872 bp
Lokacija gena (miš)
Hrom.	Hromosom 5 (miš)
Kraj	33,894,412 bp
Obrazac RNK ekspresije
	; ;
	Više referentnih podataka o ekspresiji
Ontologija gena
Molekularna funkcija	• aktivnost sa transferazom; • nucleotide binding; • protein kinase activity; • kinase activity; • GO:0001948, GO:0016582 vezivanje za proteine; • transmembrane receptor protein tyrosine kinase activity; • fibroblast growth factor binding; • fibroblast growth factor-activated receptor activity; • ATP binding; • protein tyrosine kinase activity; • phosphatidylinositol-4,5-bisphosphate 3-kinase activity; • 1-phosphatidylinositol-3-kinase activity; • vezivanje identičnih proteina; • Receptorska tirozin-kinaza; • transmembrane signaling receptor activity;
Ćelijska komponenta	• citoplazma; • integral component of membrane; • Golđijev aparat; • membrana; • focal adhesion; • ćelijska membrana; • integral component of plasma membrane; • transport vesicle; • extracellular region; • cell surface; • Endoplazmatski retikulum; • GO:0016023 citoplazmatska vezikula; • jedro; • receptor complex;
Biološki proces	• bone mineralization; • chondrocyte differentiation; • Fosforilacija; • negative regulation of developmental growth; • cell-cell signaling; • bone morphogenesis; • endochondral ossification; • bone maturation; • fibroblast growth factor receptor apoptotic signaling pathway; • MAPK cascade; • positive regulation of phosphatidylinositol 3-kinase activity; • positive regulation of phospholipase activity; • fibroblast growth factor receptor signaling pathway; • protein phosphorylation; • chondrocyte proliferation; • positive regulation of cell population proliferation; • positive regulation of ERK1 and ERK2 cascade; • protein autophosphorylation; • peptidyl-tyrosine phosphorylation; • endochondral bone growth; • positive regulation of MAPK cascade; • GO:0097285 apoptoza; • phosphatidylinositol phosphate biosynthetic process; • phosphatidylinositol-3-phosphate biosynthetic process; • positive regulation of tyrosine phosphorylation of STAT protein; • skeletal system development; • positive regulation of protein kinase B signaling; • negative regulation of signal transduction; • Ćelijska diferencijacija; • negative regulation of apoptotic process; • transmembrane receptor protein tyrosine kinase signaling pathway;
	Izvori:Amigo / QuickGO
Ortolozi
	2261
	14184
	ENSG00000068078
	ENSMUSG00000054252
	P22607
	Q61851
	NM_000142; NM_001163213; NM_022965; NM_001354809; NM_001354810
NM_001163215; NM_001163216; NM_001163217; NM_001205270; NM_008010;
	NM_001359036; NM_001359037
	NP_000133; NP_001156685; NP_075254; NP_001341738; NP_001341739
	n/a
	Wikipodaci
Pogledaj/uredi – čovjek	Pogledaj/uredi – miš

Receptor fibroblastnog faktora rasta 3 jest protein i enzim koji je kod ljudi kodiran genom FGFR3 sa hromosoma 4, pozicija p16.3.^[5] FGFR3 je također označen kao CD333 (klaster diferencijacije 333). Gen eksprimiran je u tkivima i organima kao što su hrskavica, mozak, crijeva i bubrezi.^[6]

Aminokiselinska sekvenca

Dužina polipeptidnog lanca je 806 aminokiselina, а molekulska težina 87.710 Da.^[7]

C: Cistein

D: Asparaginska kiselina

E: Glutaminska kiselina

F: Fenilalanin

G: Glicin

H: Histidin

I: Izoleucin

K: Lizin

L: Leucin

M: Metionin

N: Asparagin

P: Prolin

Q: Glutamin

R: Arginin

S: Serin

T: Treonin

V: Valin

W: Triptofan

Y: Tirozin

10	20	30	40	50
MGAPACALAL	CVAVAIVAGA	SSESLGTEQR	VVGRAAEVPG	PEPGQQEQLV
FGSGDAVELS	CPPPGGGPMG	PTVWVKDGTG	LVPSERVLVG	PQRLQVLNAS
HEDSGAYSCR	QRLTQRVLCH	FSVRVTDAPS	SGDDEDGEDE	AEDTGVDTGA
PYWTRPERMD	KKLLAVPAAN	TVRFRCPAAG	NPTPSISWLK	NGREFRGEHR
IGGIKLRHQQ	WSLVMESVVP	SDRGNYTCVV	ENKFGSIRQT	YTLDVLERSP
HRPILQAGLP	ANQTAVLGSD	VEFHCKVYSD	AQPHIQWLKH	VEVNGSKVGP
DGTPYVTVLK	TAGANTTDKE	LEVLSLHNVT	FEDAGEYTCL	AGNSIGFSHH
SAWLVVLPAE	EELVEADEAG	SVYAGILSYG	VGFFLFILVV	AAVTLCRLRS
PPKKGLGSPT	VHKISRFPLK	RQVSLESNAS	MSSNTPLVRI	ARLSSGEGPT
LANVSELELP	ADPKWELSRA	RLTLGKPLGE	GCFGQVVMAE	AIGIDKDRAA
KPVTVAVKML	KDDATDKDLS	DLVSEMEMMK	MIGKHKNIIN	LLGACTQGGP
LYVLVEYAAK	GNLREFLRAR	RPPGLDYSFD	TCKPPEEQLT	FKDLVSCAYQ
VARGMEYLAS	QKCIHRDLAA	RNVLVTEDNV	MKIADFGLAR	DVHNLDYYKK
TTNGRLPVKW	MAPEALFDRV	YTHQSDVWSF	GVLLWEIFTL	GGSPYPGIPV
EELFKLLKEG	HRMDKPANCT	HDLYMIMREC	WHAAPSQRPT	FKQLVEDLDR
VLTVTSTDEY	LDLSAPFEQY	SPGGQDTPSS	SSSGDDSVFA	HDLLPPAPPS
SGGSRT

Funkcija

Gen FGFR3 proizvodi različite oblike proteina FGFR3; lokacija varira u zavisnosti od izoforme proteina FGFR3. Budući da se različiti oblici nalaze u različitim tkivima, protein je odgovoran za višestruke interakcije faktora rasta.^[8] Mutacije funkcije u FGFR3 inhibiraju proliferaciju hondrocita i u osnovi je ahondroplazije i hipohondroplazije

Protein kodiran ovim genom je član porodice receptora faktora rasta fibroblast, gdje je sekvenca aminokiselina visoko konzervirana između članova i tokom evolucije. Članovi porodice FGFR međusobno se razlikuju po svojim afinitetnim ligandima afinit i tkivnoj distribuciji . Reprezentativni protein pune dužine sastojao bi se od vanćelijske regije, od tri domena slična imunoglobulinu, jednog hidrofobnog segmenta koji pokriva membranu i citoplazmatskog domena tirozin-kinaza. Vanćelijski dio proteina stupa u interakciju sa faktorom rasta fibroblasta, pokrećući kaskadu nizvodnih signala koji na kraju utiču na mitogenezu i diferencijaciju ćelija.

Ovaj član porodice vezuje i kiseli i osnovni faktor rasta fibroblasta i ima ulogu u razvoju i održavanju kostiju. Protein FGFR3 ima ulogu u rastu kostiju, regulacijom okoštavanja.^[8] Dešava se alternativna prerada primarnog transkripta i opisane su dodatne varijante, uključujući one koje koriste alternativni egzon 8 a ne 9, ali njihova priroda pune dužine nije utvrđena.^[9]

Mutacije

Pojednostavljenje je na mutaciji 46 XX 4p16.3 (žene), 46XY 4p16.3 (muškarci). Mutacije za dobijanje funkcije u ovom genu mogu razviti disfunkcionalne proteine "ometati rast i razvoj hrskavice i uticati na proliferaciju i kalcifikaciju hondrocita"^[6] što može dovesti do kraniosinostoze i više TIPOVA skeletne displazije (osteohondrodisplazija).

Kod ahondroplazije, gen FGFR3 ima misens mutaciju na nukleotidu 1138 koja je rezultat izmjene ili G > A ili G > C.^[10] Ova tačkasta mutacija u genu FGFR3 uzrokuje formiranje vodikovih veza između dva bočna lanca arginina što dovodi do stabilizacije dimera FGFR3 neovisne o ligandu. Prekomjerna aktivnost FGFR3 inhibira proliferaciju hondrocita i ograničava dužinu dugih kostiju.^[8]

FGFR3 mutacije su također povezane sa spermatocitnim tumorom, koji se češće javlja kod starijih muškaraca.^[11]

Klinički znmačaj

Defekti u genu FGFR3 su povezani sa nekoliko stanja, uključujući kraniosinostozu i seborejsku keratozu.^[12]

Rak mokraćne bešike

Mutacije FGFR3, fuzijskih proteina FGFR3–TACC3 i FGFR3–BAIAP2L1 često se povezuju sa rakom mjehura, dok su neke mutacije FGFR3 također povezane sa boljom prognozom. Stoga FGFR3 predstavlja potencijalnu terapijsku metu za liječenje raka mokraćne bešike.^[13]

Posttranslacijska modifikacija FGFR3 javlja se kod raka mokraćne bešike koja se ne javlja u normalnim ćelijama i može biti meta imunoterapijskih antitijela.^[14]

Glioblastom

Fuzije FGFR3-TACC3 su identificirane kao primarni mitogeni pokretači u podskupini glioblastoma (otprilike 4%) i drugih glioma i mogu biti povezani s neznatno poboljšanim ukupnim preživljavanjem.^[15] Fuzija FGFR3-TACC3 predstavlja moguću terapijsku metu kod glioblastoma.

Ahondroplazija

Ahondroplazija je dominantni genetički poremećaj uzrokovan mutacijama u FGFR3, koje čine rezultirajući protein preaktivnim. Osobe sa ovom mutacijom imaju znatno veću glavu od normalne i znatno su manje visine.^[16]^[17] Samo jedna kopija mutiranog gena FGFR3 dovodi do ahondroplazije.^[18] Obično je uzrokovana spontanim mutacijama u zametnim ćelijama; otprilike 80 % roditelja s djecom koja imaju ovaj poremećaj imaju glavu normalne veličine.^[17]^[18]

Tanatoforna displazija

Tanatoforna displazija je genetički poremećaj uzrokovan mutacija sa dobitkom funkcije u FGFR3 koji je često fatalan tokom perinatusnog perioda jer dijete ne može disati.^[19]^[20] Postoje dvije vrste. TD tip I je uzrokovan mutacijom stop kodona koja se nalazi u dijelu gena koji kodira ekstracelularni domen proteina.^[19] TD tip II je rezultat supstitucije u Lsy650Glu koji se nalazi u područje tirozin kinaze FGFR3.^[19]

Interakcije

Pokazalo se da receptor faktora rasta fibroblasta 3 ima interakcije sa FGF8^[21]^[22] i FGF9.^[21]^[22]

Također pogledate

Reference

^ ^a ^b ^c GRCh38: Ensembl release 89: ENSG00000068078 - Ensembl, maj 2017
^ ^a ^b ^c GRCm38: Ensembl release 89: ENSMUSG00000054252 - Ensembl, maj 2017
^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ Keegan K, Johnson DE, Williams LT, Hayman MJ (februar 1991). "Isolation of an additional member of the fibroblast growth factor receptor family, FGFR-3". Proceedings of the National Academy of Sciences of the United States of America. 88 (4): 1095–9. Bibcode:1991PNAS...88.1095K. doi:10.1073/pnas.88.4.1095. PMC 50963. PMID 1847508.
^ ^a ^b Wang Y, Liu Z, Liu Z, Zhao H, Zhou X, Cui Y, Han J (maj 2013). "Advances in research on and diagnosis and treatment of achondroplasia in China". Intractable & Rare Diseases Research. 2 (2): 45–50. doi:10.5582/irdr.2013.v2.2.45. PMC 4204580. PMID 25343101.
^ "UniProt, P22607" (jezik: engleski). Pristupljeno 27. 10. 2021.
^ ^a ^b ^c "FGFR3 gene". Genetics Home Reference. U.S. National Library of Medicine. Pristupljeno 27. 9. 2018.
^ "Entrez Gene: FGFR3 fibroblast growth factor receptor 3 (achondroplasia, thanatophoric dwarfism)".
^ Foldynova-Trantirkova S, Wilcox WR, Krejci P (januar 2012). "Sixteen years and counting: the current understanding of fibroblast growth factor receptor 3 (FGFR3) signaling in skeletal dysplasias". Human Mutation. 33 (1): 29–41. doi:10.1002/humu.21636. PMC 3240715. PMID 22045636.
^ Kelleher FC, O'Sullivan H, Smyth E, McDermott R, Viterbo A (oktobar 2013). "Fibroblast growth factor receptors, developmental corruption and malignant disease". Carcinogenesis. 34 (10): 2198–205. doi:10.1093/carcin/bgt254. PMID 23880303.
^ Hafner C, Hartmann A, Vogt T (juli 2007). "FGFR3 mutations in epidermal nevi and seborrheic keratoses: lessons from urothelium and skin". The Journal of Investigative Dermatology. 127 (7): 1572–3. doi:10.1038/sj.jid.5700772. PMID 17568799.
^ di Martino E, Tomlinson DC, Williams SV, Knowles MA (oktobar 2016). "A place for precision medicine in bladder cancer: targeting the FGFRs". Future Oncology (London, England). 12 (19): 2243–63. doi:10.2217/fon-2016-0042. PMC 5066128. PMID 27381494.
^ Oo HZ, Seiler R, Black PC, Daugaard M (oktobar 2018). "Post-translational modifications in bladder cancer: Expanding the tumor target repertoire". Urologic Oncology. 38 (12): 858–866. doi:10.1016/j.urolonc.2018.09.001. PMID 30342880. S2CID 53041768.
^ Mata, Douglas A.; Benhamida, Jamal K.; Lin, Andrew L.; Vanderbilt, Chad M.; Yang, Soo-Ryum; Villafania, Liliana B.; Ferguson, Donna C.; Jonsson, Philip; Miller, Alexandra M.; Tabar, Viviane; Brennan, Cameron W.; Moss, Nelson S.; Sill, Martin; Benayed, Ryma; Mellinghoff, Ingo K.; Rosenblum, Marc K.; Arcila, Maria E.; Ladanyi, Marc; Bale, Tejus A. (2020). "Genetic and epigenetic landscape of IDH-wildtype glioblastomas with FGFR3-TACC3 fusions". Acta Neuropathologica Communications. 8 (1): 186. doi:10.1186/s40478-020-01058-6. PMC 7653727. PMID 33168106.
^ "Achondroplasia". Genetic and Rare Diseases Information Center (GARD).
^ ^a ^b "FGFR3 gene". Genetics Home Reference. U.S. National Library of Medicine.
^ ^a ^b "Learning about Achondroplasia". National Human Genome Research Institute. Pristupljeno 15. 7. 2016.
^ ^a ^b ^c Karczeski B, Cutting GR (1993). Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (ured.). Thanatophoric Dysplasia. GeneReviews. University of Washington, Seattle. PMID 20301540. Pristupljeno 17. 11. 2018.
^ Nissenbaum M, Chung SM, Rosenberg HK, Buck BE (august 1977). "Thanatophoric dwarfism. Two case reports and survey of the literature". Clinical Pediatrics. 16 (8): 690–7. doi:10.1177/000992287701600803. PMID 872478. S2CID 30837380.
^ ^a ^b Santos-Ocampo S, Colvin JS, Chellaiah A, Ornitz DM (januar 1996). "Expression and biological activity of mouse fibroblast growth factor-9". The Journal of Biological Chemistry. 271 (3): 1726–31. doi:10.1074/jbc.271.3.1726. PMID 8576175.
^ ^a ^b Chellaiah A, Yuan W, Chellaiah M, Ornitz DM (decembar 1999). "Mapping ligand binding domains in chimeric fibroblast growth factor receptor molecules. Multiple regions determine ligand binding specificity". The Journal of Biological Chemistry. 274 (49): 34785–94. doi:10.1074/jbc.274.49.34785. PMID 10574949.

Dopunska literatura

Duperret EK, Oh SJ, McNeal A, Prouty SM, Ridky TW (2014). "Activating FGFR3 mutations cause mild hyperplasia in human skin, but are insufficient to drive benign or malignant skin tumors". Cell Cycle. 13 (10): 1551–9. doi:10.4161/cc.28492. PMC 4050160. PMID 24626198.
Schweitzer DN, Graham JM, Lachman RS, Jabs EW, Okajima K, Przylepa KA, Shanske A, Chen K, Neidich JA, Wilcox WR (januar 2001). "Subtle radiographic findings of achondroplasia in patients with Crouzon syndrome with acanthosis nigricans due to an Ala391Glu substitution in FGFR3". American Journal of Medical Genetics. 98 (1): 75–91. doi:10.1002/1096-8628(20010101)98:1<75::AID-AJMG1010>3.0.CO;2-6. PMID 11426459.
Horton WA, Lunstrum GP (decembar 2002). "Fibroblast growth factor receptor 3 mutations in achondroplasia and related forms of dwarfism". Reviews in Endocrine & Metabolic Disorders. 3 (4): 381–5. doi:10.1023/A:1020914026829. PMID 12424440. S2CID 7425804.
Bonaventure J, Silve C (novembar 2005). "[Hereditary skeletal dysplasias and FGFR3 and PTHR1 signaling pathways]". Médecine/Sciences. 21 (11): 954–61. doi:10.1051/medsci/20052111954. PMID 16274647.
Hernández S, Toll A, Baselga E, Ribé A, Azua-Romeo J, Pujol RM, Real FX (juli 2007). "Fibroblast growth factor receptor 3 mutations in epidermal nevi and associated low grade bladder tumors". The Journal of Investigative Dermatology. 127 (7): 1664–6. doi:10.1038/sj.jid.5700705. PMID 17255960.
Olsen SK, Ibrahimi OA, Raucci A, Zhang F, Eliseenkova AV, Yayon A, Basilico C, Linhardt RJ, Schlessinger J, Mohammadi M (januar 2004). "Insights into the molecular basis for fibroblast growth factor receptor autoinhibition and ligand-binding promiscuity". Proceedings of the National Academy of Sciences of the United States of America. 101 (4): 935–40. Bibcode:2004PNAS..101..935O. doi:10.1073/pnas.0307287101. PMC 327120. PMID 14732692.

Vanjski linkovi

GeneReviews/NIH/NCBI/UW entry on FGFR-Related Craniosynostosis Syndromes
GeneReviews/NIH/NCBI/UW entry on Muenke Syndrome
GeneReviews/NIH/NCBI/UW entry on Hypochondroplasia
FGFR3 protein, human na US National Library of Medicine Medical Subject Headings (MeSH)
P22607

Ovaj članak uključuje tekst iz Nacionalne medicinske biblioteke Sjedinjenih Država, koji je u javnom vlasništvu.

Portal Biologija

[refGRCh38Ensembl-1] GRCh38: Ensembl release 89: ENSG00000068078 - Ensembl, maj 2017

[refGRCm38Ensembl-2] GRCm38: Ensembl release 89: ENSMUSG00000054252 - Ensembl, maj 2017

[3] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[4] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[pmid1847508-5] Keegan K, Johnson DE, Williams LT, Hayman MJ (februar 1991). "Isolation of an additional member of the fibroblast growth factor receptor family, FGFR-3". Proceedings of the National Academy of Sciences of the United States of America. 88 (4): 1095–9. Bibcode:1991PNAS...88.1095K. doi:10.1073/pnas.88.4.1095. PMC 50963. PMID 1847508.

[Wang_2013-6] Wang Y, Liu Z, Liu Z, Zhao H, Zhou X, Cui Y, Han J (maj 2013). "Advances in research on and diagnosis and treatment of achondroplasia in China". Intractable & Rare Diseases Research. 2 (2): 45–50. doi:10.5582/irdr.2013.v2.2.45. PMC 4204580. PMID 25343101.

[UniProt-7] "UniProt, P22607" (jezik: engleski). Pristupljeno 27. 10. 2021.

[GHR_FGFR3-8] "FGFR3 gene". Genetics Home Reference. U.S. National Library of Medicine. Pristupljeno 27. 9. 2018.

[9] "Entrez Gene: FGFR3 fibroblast growth factor receptor 3 (achondroplasia, thanatophoric dwarfism)".

[Foldynova-Trantirkova_2012-10] Foldynova-Trantirkova S, Wilcox WR, Krejci P (januar 2012). "Sixteen years and counting: the current understanding of fibroblast growth factor receptor 3 (FGFR3) signaling in skeletal dysplasias". Human Mutation. 33 (1): 29–41. doi:10.1002/humu.21636. PMC 3240715. PMID 22045636.

[Kelleher_2013-11] Kelleher FC, O'Sullivan H, Smyth E, McDermott R, Viterbo A (oktobar 2013). "Fibroblast growth factor receptors, developmental corruption and malignant disease". Carcinogenesis. 34 (10): 2198–205. doi:10.1093/carcin/bgt254. PMID 23880303.

[Hafner_2007-12] Hafner C, Hartmann A, Vogt T (juli 2007). "FGFR3 mutations in epidermal nevi and seborrheic keratoses: lessons from urothelium and skin". The Journal of Investigative Dermatology. 127 (7): 1572–3. doi:10.1038/sj.jid.5700772. PMID 17568799.

[pmid27381494-13] Martino E, Tomlinson DC, Williams SV, Knowles MA (oktobar 2016). "A place for precision medicine in bladder cancer: targeting the FGFRs". Future Oncology (London, England). 12 (19): 2243–63. doi:10.2217/fon-2016-0042. PMC 5066128. PMID 27381494.

[pmid30342880-14] Oo HZ, Seiler R, Black PC, Daugaard M (oktobar 2018). "Post-translational modifications in bladder cancer: Expanding the tumor target repertoire". Urologic Oncology. 38 (12): 858–866. doi:10.1016/j.urolonc.2018.09.001. PMID 30342880. S2CID 53041768.

[15] Mata, Douglas A.; Benhamida, Jamal K.; Lin, Andrew L.; Vanderbilt, Chad M.; Yang, Soo-Ryum; Villafania, Liliana B.; Ferguson, Donna C.; Jonsson, Philip; Miller, Alexandra M.; Tabar, Viviane; Brennan, Cameron W.; Moss, Nelson S.; Sill, Martin; Benayed, Ryma; Mellinghoff, Ingo K.; Rosenblum, Marc K.; Arcila, Maria E.; Ladanyi, Marc; Bale, Tejus A. (2020). "Genetic and epigenetic landscape of IDH-wildtype glioblastomas with FGFR3-TACC3 fusions". Acta Neuropathologica Communications. 8 (1): 186. doi:10.1186/s40478-020-01058-6. PMC 7653727. PMID 33168106.

[GARD_Achondroplasia-16] "Achondroplasia". Genetic and Rare Diseases Information Center (GARD).

[GHR_FGFR3-17] "FGFR3 gene". Genetics Home Reference. U.S. National Library of Medicine.

[NHGRI_Achondroplasia-18] "Learning about Achondroplasia". National Human Genome Research Institute. Pristupljeno 15. 7. 2016.

[TDgenereviews-19] Karczeski B, Cutting GR (1993). Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (ured.). Thanatophoric Dysplasia. GeneReviews. University of Washington, Seattle. PMID 20301540. Pristupljeno 17. 11. 2018.

[Nissenbaum-20] Nissenbaum M, Chung SM, Rosenberg HK, Buck BE (august 1977). "Thanatophoric dwarfism. Two case reports and survey of the literature". Clinical Pediatrics. 16 (8): 690–7. doi:10.1177/000992287701600803. PMID 872478. S2CID 30837380.

[pmid8576175-21] Santos-Ocampo S, Colvin JS, Chellaiah A, Ornitz DM (januar 1996). "Expression and biological activity of mouse fibroblast growth factor-9". The Journal of Biological Chemistry. 271 (3): 1726–31. doi:10.1074/jbc.271.3.1726. PMID 8576175.

[pmid10574949-22] Chellaiah A, Yuan W, Chellaiah M, Ornitz DM (decembar 1999). "Mapping ligand binding domains in chimeric fibroblast growth factor receptor molecules. Multiple regions determine ligand binding specificity". The Journal of Biological Chemistry. 274 (49): 34785–94. doi:10.1074/jbc.274.49.34785. PMID 10574949.

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