FHIT: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
(Created page with "__NOTOC__ {{SI}} {{CMG}} {{SK}} Fragile histidine triad; bis(5'-adenosyl)-triphosphatase, human accelerated region 10 ==Overview== Fragile histidine triad protein (FHIT) is ...")
 
m (Bot: HTTP→HTTPS)
 
Line 1: Line 1:
__NOTOC__
{{Infobox_gene}}
{{SI}}
'''Bis(5'-adenosyl)-triphosphatase''' also known as '''fragile histidine triad protein''' (FHIT) is an [[enzyme]] that in humans is encoded by the ''FHIT'' [[gene]].<ref name="pmid8598045">{{cite journal | vauthors = Ohta M, Inoue H, Cotticelli MG, Kastury K, Baffa R, Palazzo J, Siprashvili Z, Mori M, McCue P, Druck T, Croce CM, Huebner K | title = The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma-associated t(3;8) breakpoint, is abnormal in digestive tract cancers | journal = Cell | volume = 84 | issue = 4 | pages = 587–97  | date = Apr 1996 | pmid = 8598045 | pmc =  | doi = 10.1016/S0092-8674(00)81034-X }}</ref><ref name="pmid9671749">{{cite journal | vauthors = Pekarsky Y, Campiglio M, Siprashvili Z, Druck T, Sedkov Y, Tillib S, Draganescu A, Wermuth P, Rothman JH, Huebner K, Buchberg AM, Mazo A, Brenner C, Croce CM | title = Nitrilase and Fhit homologs are encoded as fusion proteins in Drosophila melanogaster and Caenorhabditis elegans | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 95 | issue = 15 | pages = 8744–9  | date = Aug 1998 | pmid = 9671749 | pmc = 21147 | doi = 10.1073/pnas.95.15.8744 }}</ref>
{{CMG}}


{{SK}} Fragile histidine triad; bis(5'-adenosyl)-triphosphatase, human accelerated region 10
== Function ==


==Overview==
FHIT is also known as [[human accelerated regions|human accelerated region]] 10.  It may, therefore, have played a key role in differentiating humans from apes.<ref name="Pollard2006">{{cite journal | vauthors = Pollard KS, Salama SR, Lambert N, Lambot MA, Coppens S, Pedersen JS, Katzman S, King B, Onodera C, Siepel A, Kern AD, Dehay C, Igel H, Ares M, Vanderhaeghen P, Haussler D | title = An RNA gene expressed during cortical development evolved rapidly in humans | journal = Nature | volume = 443 | issue = 7108 | pages = 167–72  | date = 2006-08-16 | pmid = 16915236 | doi = 10.1038/nature05113 }} [http://www.nature.com/nature/journal/v443/n7108/extref/nature05113-s1.doc supplement]</ref>
Fragile histidine triad protein (FHIT) is an [[enzyme]] that in humans is encoded by the ''FHIT'' [[gene]].<ref name="pmid8598045">{{cite journal | author = Ohta M, Inoue H, Cotticelli MG, Kastury K, Baffa R, Palazzo J, Siprashvili Z, Mori M, McCue P, Druck T, Croce CM, Huebner K | title = The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma-associated t(3;8) breakpoint, is abnormal in digestive tract cancers | journal = Cell | volume = 84 | issue = 4 | pages = 587–97 |date=Apr 1996 | pmid = 8598045 | pmc =  | doi =10.1016/S0092-8674(00)81034-X  }}</ref><ref name="pmid9671749">{{cite journal | author = Pekarsky Y, Campiglio M, Siprashvili Z, Druck T, Sedkov Y, Tillib S, Draganescu A, Wermuth P, Rothman JH, Huebner K, Buchberg AM, Mazo A, Brenner C, Croce CM | title = Nitrilase and Fhit homologs are encoded as fusion proteins in Drosophila melanogaster and Caenorhabditis elegans | journal = Proc Natl Acad Sci U S A | volume = 95 | issue = 15 | pages = 8744–9 |date=Aug 1998 | pmid = 9671749 | pmc = 21147 | doi =10.1073/pnas.95.15.8744  }}</ref>  FHIT is also known as [[human accelerated regions|human accelerated region]] 10; it may, therefore, have played a key role in differentiating humans from apes.<ref name="Pollard2006">{{cite journal |author=Pollard KS, Salama SR, Lambert N, Lambot MA, Coppens S, Pedersen JS, Katzman S, King B, Onodera C, Siepel A, Kern AD, Dehay C, Igel H, Ares M Jr, Vanderhaeghen P, Haussler D |title=An RNA gene expressed during cortical development evolved rapidly in humans |journal=Nature |volume=443 |issue=7108 |pages=167–172 |date=2006-08-16 |pmid=16915236 |doi=10.1038/nature05113}} [http://www.nature.com/nature/journal/v443/n7108/extref/nature05113-s1.doc supplement]</ref>  FHIT gene, a member of the histidine triad gene family, encodes a diadenosine P1,P3-bis(5'-adenosyl)-triphosphate adenylohydrolase involved in [[purine metabolism]]. The gene encompasses the common fragile site FRA3B on chromosome 3, where [[carcinogen]]-induced damage can lead to translocations and aberrant transcripts of this gene. In fact, aberrant transcripts from this gene have been found in about half of all esophageal, stomach, and colon [[carcinoma]]s.<ref>{{cite web | title = Entrez Gene: FHIT fragile histidine triad gene| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2272| accessdate = }}</ref>  Although the exact molecular function of FHIT is still partially unclear, the gene works as a [[tumor suppressor gene|tumor suppressor]] as it has been demonstrated in animal studies.<ref name="pmid10758156">{{cite journal | author = Fong LY, Fidanza V, Zanesi N, Lock LF, Siracusa LD, Mancini R, Siprashvili Z, Ottey M, Martin SE, Druck T, McCue PA, Croce CM, Huebner K | title = Muir-Torre-like syndrome in Fhit-deficient mice | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 97 | issue = 9 | pages = 4742–7 |date=April 2000 | pmid = 10758156 | pmc = 18303 | doi = 10.1073/pnas.080063497 | url = | issn = }}</ref><ref name="pmid11517343">{{cite journal | author = Zanesi N, Fidanza V, Fong LY, Mancini R, Druck T, Valtieri M, Rüdiger T, McCue PA, Croce CM, Huebner K | title = The tumor spectrum in FHIT-deficient mice | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 98 | issue = 18 | pages = 10250–5 |date=August 2001 | pmid = 11517343 | pmc = 56947 | doi = 10.1073/pnas.191345898 | url = | issn = }}</ref><ref name="pmid16085127">{{cite journal | author = Zanesi N, Pekarsky Y, Croce CM | title = A mouse model of the fragile gene FHIT: From carcinogenesis to gene therapy and cancer prevention | journal = Mutat. Res. | volume = 591 | issue = 1-2 | pages = 103–9 |date=December 2005 | pmid = 16085127 | doi = 10.1016/j.mrfmmm.2005.05.016 | url = | issn = }}</ref> Furthermore FHIT has been shown to synergize with [[VHL gene|VHL]], another tumor suppressor, in protecting against chemically - induced lung cancer.<ref name="pmid16061637">{{cite journal | author = Zanesi N, Mancini R, Sevignani C, Vecchione A, Kaou M, Valtieri M, Calin GA, Pekarsky Y, Gnarra JR, Croce CM, Huebner K | title = Lung cancer susceptibility in Fhit-deficient mice is increased by Vhl haploinsufficiency | journal = Cancer Res. | volume = 65 | issue = 15 | pages = 6576–82 |date=August 2005 | pmid = 16061637 | doi = 10.1158/0008-5472.CAN-05-1128 | url = | issn = }}</ref>  FHIT also acts as a tumor suppressor of [[HER2/neu]] driven breast cancer.<ref name="pmid17374991">{{cite journal | author = Bianchi F, Tagliabue E, Ménard S, Campiglio M | title = Fhit expression protects against HER2-driven breast tumor development: unraveling the molecular interconnections | journal = Cell Cycle | volume = 6 | issue = 6 | pages = 643–6 |date=March 2007 | pmid = 17374991 | doi = 10.4161/cc.6.6.4033| url = | issn = }}</ref>  FHIT has been shown to [[Protein-protein interaction|interact]] with [[UBE2I]].<ref name="pmid11085938">{{cite journal | author = Shi Y, Zou M, Farid NR, Paterson MC | title = Association of FHIT (fragile histidine triad), a candidate tumour suppressor gene, with the ubiquitin-conjugating enzyme hUBC9 | journal = Biochem. J. | volume = 352 | issue = 2| pages = 443–8 |date=December 2000 | pmid = 11085938 | pmc = 1221476 | doi = 10.1042/0264-6021:3520443| url = | issn = }}</ref>


==References==
This gene, a member of the histidine triad gene family, encodes a diadenosine 
{{Reflist|2}}
P1,P3-bis(5'-adenosyl)-triphosphate adenylohydrolase involved in [[purine metabolism]]. The gene encompasses the common fragile site FRA3B on chromosome 3, where [[carcinogen]]-induced damage can lead to translocations and aberrant transcripts of this gene. In fact, aberrant transcripts from this gene have been found in about half of all esophageal, stomach, and colon [[carcinoma]]s.<ref>{{cite web | title = Entrez Gene: FHIT fragile histidine triad gene| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2272| accessdate = }}</ref>
 
Though the exact molecular function of FHIT is still partially unclear, the gene works as a [[tumor suppressor gene|tumor suppressor]] as it has been demonstrated in animal studies.<ref name="pmid10758156">{{cite journal | vauthors = Fong LY, Fidanza V, Zanesi N, Lock LF, Siracusa LD, Mancini R, Siprashvili Z, Ottey M, Martin SE, Druck T, McCue PA, Croce CM, Huebner K | title = Muir-Torre-like syndrome in Fhit-deficient mice | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 97 | issue = 9 | pages = 4742–7  | date = April 2000 | pmid = 10758156 | pmc = 18303 | doi = 10.1073/pnas.080063497 }}</ref><ref name="pmid11517343">{{cite journal | vauthors = Zanesi N, Fidanza V, Fong LY, Mancini R, Druck T, Valtieri M, Rüdiger T, McCue PA, Croce CM, Huebner K | title = The tumor spectrum in FHIT-deficient mice | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 98 | issue = 18 | pages = 10250–5  | date = August 2001 | pmid = 11517343 | pmc = 56947 | doi = 10.1073/pnas.191345898 }}</ref><ref name="pmid16085127">{{cite journal | vauthors = Zanesi N, Pekarsky Y, Croce CM | title = A mouse model of the fragile gene FHIT: From carcinogenesis to gene therapy and cancer prevention | journal = Mutat. Res. | volume = 591 | issue = 1-2 | pages = 103–9  | date = December 2005 | pmid = 16085127 | doi = 10.1016/j.mrfmmm.2005.05.016 }}</ref> Furthermore FHIT has been shown to synergize with [[Von Hippel–Lindau tumor suppressor|VHL]], another tumor suppressor, in protecting against chemically - induced lung cancer.<ref name="pmid16061637">{{cite journal | vauthors = Zanesi N, Mancini R, Sevignani C, Vecchione A, Kaou M, Valtieri M, Calin GA, Pekarsky Y, Gnarra JR, Croce CM, Huebner K | title = Lung cancer susceptibility in Fhit-deficient mice is increased by Vhl haploinsufficiency | journal = Cancer Res. | volume = 65 | issue = 15 | pages = 6576–82  | date = August 2005 | pmid = 16061637 | doi = 10.1158/0008-5472.CAN-05-1128 }}</ref>
 
FHIT also acts as a tumor suppressor of [[HER2/neu]] driven breast cancer.<ref name="pmid17374991">{{cite journal | vauthors = Bianchi F, Tagliabue E, Ménard S, Campiglio M | title = Fhit expression protects against HER2-driven breast tumor development: unraveling the molecular interconnections | journal = Cell Cycle | volume = 6 | issue = 6 | pages = 643–6  | date = March 2007 | pmid = 17374991 | doi = 10.4161/cc.6.6.4033 }}</ref>
 
== Interactions ==
 
FHIT has been shown to [[Protein-protein interaction|interact]] with [[UBE2I]].<ref name="pmid11085938">{{cite journal | vauthors = Shi Y, Zou M, Farid NR, Paterson MC | title = Association of FHIT (fragile histidine triad), a candidate tumour suppressor gene, with the ubiquitin-conjugating enzyme hUBC9 | journal = Biochem. J. | volume = 352 Pt 2 | issue = 2 | pages = 443–8  | date = December 2000 | pmid = 11085938 | pmc = 1221476 | doi = 10.1042/0264-6021:3520443 }}</ref>
 
== References ==
{{reflist}}
 
{{PDB Gallery|geneid=2272}}
 
 
{{gene-3-stub}}

Latest revision as of 04:48, 31 August 2017

VALUE_ERROR (nil)
Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

n/a

n/a

Ensembl

n/a

n/a

UniProt

n/a

n/a

RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

Bis(5'-adenosyl)-triphosphatase also known as fragile histidine triad protein (FHIT) is an enzyme that in humans is encoded by the FHIT gene.[1][2]

Function

FHIT is also known as human accelerated region 10. It may, therefore, have played a key role in differentiating humans from apes.[3]

This gene, a member of the histidine triad gene family, encodes a diadenosine P1,P3-bis(5'-adenosyl)-triphosphate adenylohydrolase involved in purine metabolism. The gene encompasses the common fragile site FRA3B on chromosome 3, where carcinogen-induced damage can lead to translocations and aberrant transcripts of this gene. In fact, aberrant transcripts from this gene have been found in about half of all esophageal, stomach, and colon carcinomas.[4]

Though the exact molecular function of FHIT is still partially unclear, the gene works as a tumor suppressor as it has been demonstrated in animal studies.[5][6][7] Furthermore FHIT has been shown to synergize with VHL, another tumor suppressor, in protecting against chemically - induced lung cancer.[8]

FHIT also acts as a tumor suppressor of HER2/neu driven breast cancer.[9]

Interactions

FHIT has been shown to interact with UBE2I.[10]

References

  1. ↑ Ohta M, Inoue H, Cotticelli MG, Kastury K, Baffa R, Palazzo J, Siprashvili Z, Mori M, McCue P, Druck T, Croce CM, Huebner K (Apr 1996). "The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma-associated t(3;8) breakpoint, is abnormal in digestive tract cancers". Cell. 84 (4): 587–97. doi:10.1016/S0092-8674(00)81034-X. PMID 8598045.
  2. ↑ Pekarsky Y, Campiglio M, Siprashvili Z, Druck T, Sedkov Y, Tillib S, Draganescu A, Wermuth P, Rothman JH, Huebner K, Buchberg AM, Mazo A, Brenner C, Croce CM (Aug 1998). "Nitrilase and Fhit homologs are encoded as fusion proteins in Drosophila melanogaster and Caenorhabditis elegans". Proc. Natl. Acad. Sci. U.S.A. 95 (15): 8744–9. doi:10.1073/pnas.95.15.8744. PMC 21147. PMID 9671749.
  3. ↑ Pollard KS, Salama SR, Lambert N, Lambot MA, Coppens S, Pedersen JS, Katzman S, King B, Onodera C, Siepel A, Kern AD, Dehay C, Igel H, Ares M, Vanderhaeghen P, Haussler D (2006-08-16). "An RNA gene expressed during cortical development evolved rapidly in humans". Nature. 443 (7108): 167–72. doi:10.1038/nature05113. PMID 16915236. supplement
  4. ↑ "Entrez Gene: FHIT fragile histidine triad gene".
  5. ↑ Fong LY, Fidanza V, Zanesi N, Lock LF, Siracusa LD, Mancini R, Siprashvili Z, Ottey M, Martin SE, Druck T, McCue PA, Croce CM, Huebner K (April 2000). "Muir-Torre-like syndrome in Fhit-deficient mice". Proc. Natl. Acad. Sci. U.S.A. 97 (9): 4742–7. doi:10.1073/pnas.080063497. PMC 18303. PMID 10758156.
  6. ↑ Zanesi N, Fidanza V, Fong LY, Mancini R, Druck T, Valtieri M, Rüdiger T, McCue PA, Croce CM, Huebner K (August 2001). "The tumor spectrum in FHIT-deficient mice". Proc. Natl. Acad. Sci. U.S.A. 98 (18): 10250–5. doi:10.1073/pnas.191345898. PMC 56947. PMID 11517343.
  7. ↑ Zanesi N, Pekarsky Y, Croce CM (December 2005). "A mouse model of the fragile gene FHIT: From carcinogenesis to gene therapy and cancer prevention". Mutat. Res. 591 (1–2): 103–9. doi:10.1016/j.mrfmmm.2005.05.016. PMID 16085127.
  8. ↑ Zanesi N, Mancini R, Sevignani C, Vecchione A, Kaou M, Valtieri M, Calin GA, Pekarsky Y, Gnarra JR, Croce CM, Huebner K (August 2005). "Lung cancer susceptibility in Fhit-deficient mice is increased by Vhl haploinsufficiency". Cancer Res. 65 (15): 6576–82. doi:10.1158/0008-5472.CAN-05-1128. PMID 16061637.
  9. ↑ Bianchi F, Tagliabue E, Ménard S, Campiglio M (March 2007). "Fhit expression protects against HER2-driven breast tumor development: unraveling the molecular interconnections". Cell Cycle. 6 (6): 643–6. doi:10.4161/cc.6.6.4033. PMID 17374991.
  10. ↑ Shi Y, Zou M, Farid NR, Paterson MC (December 2000). "Association of FHIT (fragile histidine triad), a candidate tumour suppressor gene, with the ubiquitin-conjugating enzyme hUBC9". Biochem. J. 352 Pt 2 (2): 443–8. doi:10.1042/0264-6021:3520443. PMC 1221476. PMID 11085938.


Retrieved from "https://www.wikidoc.org/index.php?title=FHIT&oldid=1413010"