Fibroblast growth factor: Difference between revisions

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*  '''FGF2''' is called basic FGF.<br />
*  '''FGF2''' is called basic FGF.<br />
*  '''FGF4''' has multiple roles during vertebrate embryogenesis<ref>PMID:18792115</ref>.<br />
*  '''FGF4''' has multiple roles during vertebrate embryogenesis<ref>PMID:18792115</ref>.<br />
*  '''FGF7''' is called keratinocyte growth factor which is present in the epitheliazation-phase of wound healing when keratinocytes are covering the wound<ref>PMID:11052999</ref>.  FGF7 is aparacrine growth factor in the breast<ref>PMID:12697038</ref>.
*  '''FGF7''' is called '''keratinocyte growth factor''' which is present in the epitheliazation-phase of wound healing when keratinocytes are covering the wound<ref>PMID:11052999</ref>.  FGF7 is aparacrine growth factor in the breast<ref>PMID:12697038</ref>.
*  '''FGF8''' has multiple roles in the regulation of embryogenesis, cell differentiation, proliferation and migration.  It is required for normal development of normal brain, eye, ear and limb<ref>PMID:22273727</ref>.<br />
*  '''FGF8''' has multiple roles in the regulation of embryogenesis, cell differentiation, proliferation and migration.  It is required for normal development of normal brain, eye, ear and limb<ref>PMID:22273727</ref>.<br />
*  '''FGF9''' is produced and secreted by the prostatic stromal cells<ref>PMID:10362017</ref>.<br />
*  '''FGF9''' is produced and secreted by the prostatic stromal cells<ref>PMID:10362017</ref>.<br />
*  '''FGF10''' has essential role in the growth of fetal prostate <ref>PMID:12941620</ref>.<br />
*  '''FGF10''' has essential role in the growth of fetal prostate <ref>PMID:12941620</ref>.<br />
*  '''FGF12''' is a key regulator of the vascular smooth muscle cell phenotype switch<ref>PMID:27470512</ref>.<br />
*  '''FGF12''' is a key regulator of the vascular smooth muscle cell phenotype switch<ref>PMID:27470512</ref>.<br />
*  '''FGF13''' regulates proliferation and differentiation of the skeletal muscle cells <ref>PMID:26230950</ref>.<br />
*  '''FGF18''' has al role in organ development and damage repair <ref>PMID:36871047</ref>.<br />
*  '''FGF19''' has high affinity to FGFR4<ref>PMID:10525310</ref>.<br />
*  '''FGF21''' has a role in regulating body weight in a dietary carbohydrate-dependent manner <ref>PMID:37030441</ref>.<br />
*  '''FGF23''' is produced by bone cells and regulates renal phosphate and vitamin D metabolism <ref>PMID:29760049</ref>.<br />
See also [[Fibroblast growth factor receptor]] and [[Growth factors]].
== Disease ==
Mutations in '''FGF20''' are associated with Parkinson's disease<ref>PMID:2823</ref>.


== Relevance ==
== Relevance ==


'''FGF''' signaling is important in the pathogenesis of a variety of tumor types<ref>PMID:20094046</ref>, angiogenesis<ref>PMID:7542215</ref> and wound healing<ref>PMID:12696985</ref>.  '''FGF1''' is a potentially safw candidate for restoring euglycaemia without causing a=overt adverse effects<ref>PMID:28664920</ref>.  Overexpression of the high molecular weight isoform of '''FGF2''' in bone results in catabolic activity in joint cartilage and bone that leads to osteoarthropathy<ref>PMID:27732085</ref>.  '''FGF12''' could be a therapeutic target for treating restenosis and atherosclerosis.
'''FGF''' signaling is important in the pathogenesis of a variety of tumor types<ref>PMID:20094046</ref>, angiogenesis<ref>PMID:7542215</ref> and wound healing<ref>PMID:12696985</ref>.  '''FGF1''' is a potentially safw candidate for restoring euglycaemia without causing a=overt adverse effects<ref>PMID:28664920</ref>.  Overexpression of the high molecular weight isoform of '''FGF2''' in bone results in catabolic activity in joint cartilage and bone that leads to osteoarthropathy<ref>PMID:27732085</ref>.  '''FGF12''' could be a therapeutic target for treating restenosis and atherosclerosis. '''FGF18''' is overexpressed in ovarian cancer and hence may serve as therapeutic target<ref>PMID:24018557</ref>.  '''FGF19''' is overexpressed in lung squamous cell carcinoma and hence may serve as therapeutic target<ref>PMID:28906590</ref>.


== Structural insights ==
== Structural insights ==


<scene name='54/544711/Cv/2'>The heparin binds in the dimer interface</scene><ref>PMID:18540049</ref>.  
<scene name='54/544711/Cv/3'>The heparin binds in the dimer interface of the rat fibroblast growth factor 1</scene><ref>PMID:18540049</ref>. Water molecules are shown as red spheres.
</StructureSection>


==3D structures of fibroblast growth factor==
==3D structures of fibroblast growth factor==
[[Fibroblast growth factor 3D structures]]


Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
</StructureSection>
{{#tree:id=OrganizedByTopic|openlevels=0|
 
*FGF1
 
**[[1fmm]] – FGF1 – ''Notophthalmus viridescens'' - NMR  <br />
**[[1afc]] – bFGF1 + HS – bovine<br />
**[[1bar]] – bFGF1  <br />
**[[2j3p]] – rFGF1  - rat<br />
**[[3hal]] – FGF1 - rabbit  <br />
**[[2afg]], [[1jqz]], [[1rg8]] – hFGF1 - human <br />
**[[1jt3]], [[1jt4]], [[1jt5]], [[1jt7]], [[1jtc]], [[1k5u]], [[1k5v]], [[1m16]], [[1jy0]], [[1nzk]], [[1p63]], [[1pzz]], [[1q03]], [[1q04]], [[1yto]], [[1z2v]], [[1z4s]], [[2aqz]], [[2hw9]], [[2hwa]], [[2hwm]], [[2hz9]], [[2ntd]], [[3b9u]], [[3ba4]], [[3ba5]], [[3ba7]], [[3bad]], [[3bag]], [[3bah]], [[3bao]], [[3baq]], [[3bau]], [[3bav]], [[3bb2]], [[2q9x]], [[3crg]], [[3crh]], [[3cri]], [[3cqa]], [[3fgm]], [[3fj8]], [[3fj9]], [[3fja]], [[3fjb]], [[3fjc]], [[3fjd]], [[3fje]], [[3fjf]], [[3fjh]], [[3fji]], [[3fjj]], [[3fjk]], [[3hom]], [[3o3q]], [[4q91]], [[4q9g]], [[4q9p]], [[4qal]], [[4qbc]], [[4qbv]], [[4qc4]], [[4yol]], [[4xki]], [[4qo3]] – hFGF1 (mutant)  <br />
**[[1dzd]], [[2rq9]] – hFGF1 - NMR  <br />
**[[1dzc]] – hFGF1 (mutant) - NMR  <br />
 
*''FGF1 complex with small molecule''
 
**[[1axm]], [[2axm]] – hFGF1  + HS <br />
**[[3ud7]], [[3ud8]], [[3ud9]], [[3uda]] – hFGF1 + disaccharide  <br />
**[[2uus]] – rFGF1  + HS <br />
**[[2erm]] – hFGF1  + HS - NMR<br />
**[[1rml]] – hFGF1  + naphthalene trisulphonate - NMR  <br />
**[[1hkn]] – hFGF1  + naphthalene trisulphonate  <br />
**[[2k8r]] – hFGF1  + anti-angiogenic drug - NMR<br />
**[[3k1x]] – hFGF1  + vasoprotectant drug <br />
**[[3jut]] – hFGF1  + inhibitor  <br />
**[[2ki4]], [[2ki6]] – hFGF1  + S100-A13<br />
 
*''FGF1 complex with FGF receptor''
 
**[[1e0o]] – hFGF1 (mutant) + hFGFR2 (mutant) + HS<br />
**[[3oj2]], [[3ojm]], [[1djs]] – hFGF1 + hFGFR2 (mutant) <br />
**[[1evt]] – hFGF1 + hFGFR1 <br />
**[[3ojv]] – hFGF1 + hFGFR1 (mutant) <br />
**[[1ry7]] – hFGF1 + hFGFR3<br />
**[[3cu1]] – hFGF1 + hFGFR2<br />
**[[4j23]] – hFGF1 + hFGFR2 + inhibitor<br />
 
*FGF2
 
**[[2fgf]] – hFGF2 precursor <br />
**[[1fga]], [[4fgf]], [[1bas]], [[1bfg]], [[2bfh]], [[1bff]] – hFGF2  <br />
**[[1wvz]], [[2k43]], [[2k4a]] – hFGF2 - NMR  <br />
**[[1bla]], [[1bld]] – hFGF2 (mutant) - NMR  <br />
**[[1bfb]], [[1bfc]] – hFGF2  + heparin <br />
**[[5x1o]] – hFGF2 + inositol triphosphate <br />
**[[1cvs]] – hFGF2 (mutant) + hFGFR1 (mutant) <br />
**[[1fq9]] – hFGF2 (mutant) + hFGFR1 (mutant) + HS<br />
**[[1ev2]] - hFGF2 (mutant) + hFGFR2 <br />
**[[2m49]] - hFGF2 (mutant) + S100-B <br />
**[[4oee]], [[4oef]], [[4oeg]] - hFGF2 (mutant) + disaccharide <br />
 
*FGF4
 
**[[1ijt]] – hFGF4 b-trefoil domain <br />
 
*FGF7
 
**[[1qqk]] – rFGF7  <br />
**[[1qql]] – rFGF7/hFGF1 <br />
 
*FGF8
 
**[[2fdb]] – hFGF8b + hFGFR2  <br />
 
*FGF9
 
**[[1g82]], [[1ihk]] – hFGF9  <br />
**[[5w59]] – hFGF9 (mutant) + hFGFR1  <br />
 
*FGF10
 
**[[1nun]] – hFGF10 + hFGFR2  <br />
 
*FGF12
 
**[[1q1u]] – hFGF12 (mutant)  <br />
**[[4jq0]] – hFGF12 + calmodulin + sodium channel subunit α <br />
 
*FGF13
 
**[[3hbw]] – hFGF13  <br />
**[[4dck]], [[4jpz]] – hFGF13 + calmodulin + sodium channel subunit α <br />
 
*FGF18
 
**[[4cjm]] – hFGF18  <br />
 
*FGF19
 
**[[1pwa]], [[2p23]] – hFGF19  <br />
 
*FGF20
 
**[[3f1r]] – hFGF20  <br />
 
*FGF23


**[[2p39]] – hFGF23  <br />
**[[5w21]] – hFGF23 + klotho  <br />
}}
== References ==
== References ==
<references/>
<references/>


[[Category:Topic Page]]
[[Category:Topic Page]]

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Michal Harel, Alexander Berchansky