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{{protein
{{infobox protein
|Name=zinc metallopeptidase (STE24 homolog, S. cerevisiae)
|Name=zinc metallopeptidase (STE24 homolog, S. cerevisiae)
|caption=
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|LocusSupplementaryData=
|LocusSupplementaryData=
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{{SI}}
'''ZMPSTE24''' is a human [[gene]].<ref name="pmid9700155">{{cite journal | vauthors = Tam A, Nouvet FJ, Fujimura-Kamada K, Slunt H, Sisodia SS, Michaelis S | title = Dual roles for Ste24p in yeast a-factor maturation: NH2-terminal proteolysis and COOH-terminal CAAX processing | journal = J. Cell Biol. | volume = 142 | issue = 3 | pages = 635–49 |date=August 1998 | pmid = 9700155 | pmc = 2148179 | doi = 10.1083/jcb.142.3.635| url = http://www.jcb.org/cgi/pmidlookup?view=long&pmid=9700155 }}</ref><ref name="pmid10373325">{{cite journal | vauthors = Freije JM, Blay P, Pendás AM, Cadiñanos J, Crespo P, López-Otín C | title = Identification and chromosomal location of two human genes encoding enzymes potentially involved in proteolytic maturation of farnesylated proteins | journal = Genomics | volume = 58 | issue = 3 | pages = 270–80 |date=June 1999 | pmid = 10373325 | doi = 10.1006/geno.1999.5834 | url =  }}</ref> The [[protein]] encoded by this gene is a [[metallopeptidase]]. It is involved in the processing of [[LMNA|lamin&nbsp;A]].<ref name="pmid16207929">{{cite journal | vauthors = Young SG, Fong LG, Michaelis S | title = Prelamin A, Zmpste24, misshapen cell nuclei, and progeria--new evidence suggesting that protein farnesylation could be important for disease pathogenesis | journal = J. Lipid Res. | volume = 46 | issue = 12 | pages = 2531–58 |date=December 2005 | pmid = 16207929 | doi = 10.1194/jlr.R500011-JLR200 | url =  }}</ref> Defects in the ZMPSTE24 gene lead to similar [[laminopathy|laminopathies]] as defects in lamin&nbsp;A, because the latter is a substrate for the former.<ref name="pmid16079796">{{cite journal | vauthors = Varela I, Cadiñanos J, Pendás AM, Gutiérrez-Fernández A, Folgueras AR, Sánchez LM, Zhou Z, Rodríguez FJ, Stewart CL, Vega JA, Tryggvason K, Freije JM, López-Otín C | title = Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation | journal = Nature | volume = 437 | issue = 7058 | pages = 564–8 |date=September 2005 | pmid = 16079796 | doi = 10.1038/nature04019 }}</ref>  In humans, a mutation abolishing the ZMPSTE24 cleavage site in [[LMNA|prelamin A]] causes a [[Progeria|progeroid disorder]].<ref name="pmid27034136">{{cite journal |vauthors=Wang Y, Lichter-Konecki U, Anyane-Yeboa K, Shaw JE, Lu JT, Östlund C, Shin JY, Clark LN, Gundersen GG, Nagy PL, Worman HJ |title=A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder |journal=J. Cell Sci. |volume=129 |issue=10 |pages=1975–80 |year=2016 |pmid=27034136 |pmc=4878994 |doi=10.1242/jcs.187302 |url=}}</ref>  Failure to correctly process prelamin A leads to deficient ability to [[DNA repair|repair DNA double-strand breaks]].<ref name="pmid21701264">{{cite journal |vauthors=Redwood AB, Perkins SM, Vanderwaal RP, Feng Z, Biehl KJ, Gonzalez-Suarez I, Morgado-Palacin L, Shi W, Sage J, Roti-Roti JL, Stewart CL, Zhang J, Gonzalo S |title=A dual role for A-type lamins in DNA double-strand break repair |journal=Cell Cycle |volume=10 |issue=15 |pages=2549–60 |year=2011 |pmid=21701264 |pmc=3180193 |doi=10.4161/cc.10.15.16531 |url=}}</ref><ref name="pmid26079711">{{cite journal |vauthors=Gonzalo S, Kreienkamp R |title=DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome |journal=Curr. Opin. Cell Biol. |volume=34 |issue= |pages=75–83 |year=2015 |pmid=26079711 |pmc=4522337 |doi=10.1016/j.ceb.2015.05.007 |url=}}</ref>


 
As shown by Liu et al.,<ref name="pmid15980864">{{cite journal |vauthors=Liu B, Wang J, Chan KM, Tjia WM, Deng W, Guan X, Huang JD, Li KM, Chau PY, Chen DJ, Pei D, Pendas AM, Cadiñanos J, López-Otín C, Tse HF, Hutchison C, Chen J, Cao Y, Cheah KS, Tryggvason K, Zhou Z |title=Genomic instability in laminopathy-based premature aging |journal=Nat. Med. |volume=11 |issue=7 |pages=780–5 |year=2005 |pmid=15980864 |doi=10.1038/nm1266 |url=}}</ref> lack of Zmpste24 prevents [[LMNA|lamin A]] formation from its precursor farnesyl-prelamin A. Lack of Zmpste24 causes progeroid phenotypes in mice and humans.  This lack increases DNA damage and chromosome aberrations and sensitivity to DNA-damaging agents that cause double-strand breaks.  Also, lack of Zmpste24 allows an increase in [[non-homologous end joining]], but a deficiency in steps leading to  [[homologous recombination]]al DNA repair.
'''ZMPSTE24''' is a human [[gene]].<ref name="pmid9700155">{{cite journal | author = Tam A, Nouvet FJ, Fujimura-Kamada K, Slunt H, Sisodia SS, Michaelis S | title = Dual roles for Ste24p in yeast a-factor maturation: NH2-terminal proteolysis and COOH-terminal CAAX processing | journal = J. Cell Biol. | volume = 142 | issue = 3 | pages = 635–49 | year = 1998 | month = August | pmid = 9700155 | pmc = 2148179 | doi = | url = http://www.jcb.org/cgi/pmidlookup?view=long&pmid=9700155 | issn = }}</ref><ref name="pmid10373325">{{cite journal | author = Freije JM, Blay P, Pendás AM, Cadiñanos J, Crespo P, López-Otín C | title = Identification and chromosomal location of two human genes encoding enzymes potentially involved in proteolytic maturation of farnesylated proteins | journal = Genomics | volume = 58 | issue = 3 | pages = 270–80 | year = 1999 | month = June | pmid = 10373325 | doi = 10.1006/geno.1999.5834 | url = | issn = }}</ref> The [[protein]] encoded by this gene is a [[metallopeptidase]]. It is involved in the processing of [[Lamin A]].<ref name="pmid16207929">{{cite journal | author = Young SG, Fong LG, Michaelis S | title = Prelamin A, Zmpste24, misshapen cell nuclei, and progeria--new evidence suggesting that protein farnesylation could be important for disease pathogenesis | journal = J. Lipid Res. | volume = 46 | issue = 12 | pages = 2531–58 | year = 2005 | month = December | pmid = 16207929 | doi = 10.1194/jlr.R500011-JLR200 | url = | issn = }}</ref>


==See also==
==See also==
* [[progeria]]
* [[Progeria]]
* [[Progeroid syndromes]]


==References==
==References==
{{Reflist}}
{{Reflist}}


{{refend}}
==External links==
* {{UCSC genome browser|ZMPSTE24}}
* {{UCSC gene details|ZMPSTE24}}


{{Metalloendopeptidases}}


[[de:CAAX-Prenylprotease 1]]


{{WH}}
{{biochem-stub}}
{{WS}}

Latest revision as of 22:39, 8 November 2017

zinc metallopeptidase (STE24 homolog, S. cerevisiae)
Identifiers
SymbolZMPSTE24
Entrez10269
HUGO12877
OMIM606480
RefSeqNM_005857
UniProtO75844
Other data
EC number3.4.24.84
LocusChr. 1 p34

ZMPSTE24 is a human gene.[1][2] The protein encoded by this gene is a metallopeptidase. It is involved in the processing of lamin A.[3] Defects in the ZMPSTE24 gene lead to similar laminopathies as defects in lamin A, because the latter is a substrate for the former.[4] In humans, a mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder.[5] Failure to correctly process prelamin A leads to deficient ability to repair DNA double-strand breaks.[6][7]

As shown by Liu et al.,[8] lack of Zmpste24 prevents lamin A formation from its precursor farnesyl-prelamin A. Lack of Zmpste24 causes progeroid phenotypes in mice and humans. This lack increases DNA damage and chromosome aberrations and sensitivity to DNA-damaging agents that cause double-strand breaks. Also, lack of Zmpste24 allows an increase in non-homologous end joining, but a deficiency in steps leading to homologous recombinational DNA repair.

See also

References

  1. ↑ Tam A, Nouvet FJ, Fujimura-Kamada K, Slunt H, Sisodia SS, Michaelis S (August 1998). "Dual roles for Ste24p in yeast a-factor maturation: NH2-terminal proteolysis and COOH-terminal CAAX processing". J. Cell Biol. 142 (3): 635–49. doi:10.1083/jcb.142.3.635. PMC 2148179. PMID 9700155.
  2. ↑ Freije JM, Blay P, Pendás AM, Cadiñanos J, Crespo P, López-Otín C (June 1999). "Identification and chromosomal location of two human genes encoding enzymes potentially involved in proteolytic maturation of farnesylated proteins". Genomics. 58 (3): 270–80. doi:10.1006/geno.1999.5834. PMID 10373325.
  3. ↑ Young SG, Fong LG, Michaelis S (December 2005). "Prelamin A, Zmpste24, misshapen cell nuclei, and progeria--new evidence suggesting that protein farnesylation could be important for disease pathogenesis". J. Lipid Res. 46 (12): 2531–58. doi:10.1194/jlr.R500011-JLR200. PMID 16207929.
  4. ↑ Varela I, Cadiñanos J, Pendás AM, Gutiérrez-Fernández A, Folgueras AR, Sánchez LM, Zhou Z, Rodríguez FJ, Stewart CL, Vega JA, Tryggvason K, Freije JM, López-Otín C (September 2005). "Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation". Nature. 437 (7058): 564–8. doi:10.1038/nature04019. PMID 16079796.
  5. ↑ Wang Y, Lichter-Konecki U, Anyane-Yeboa K, Shaw JE, Lu JT, Östlund C, Shin JY, Clark LN, Gundersen GG, Nagy PL, Worman HJ (2016). "A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder". J. Cell Sci. 129 (10): 1975–80. doi:10.1242/jcs.187302. PMC 4878994. PMID 27034136.
  6. ↑ Redwood AB, Perkins SM, Vanderwaal RP, Feng Z, Biehl KJ, Gonzalez-Suarez I, Morgado-Palacin L, Shi W, Sage J, Roti-Roti JL, Stewart CL, Zhang J, Gonzalo S (2011). "A dual role for A-type lamins in DNA double-strand break repair". Cell Cycle. 10 (15): 2549–60. doi:10.4161/cc.10.15.16531. PMC 3180193. PMID 21701264.
  7. ↑ Gonzalo S, Kreienkamp R (2015). "DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome". Curr. Opin. Cell Biol. 34: 75–83. doi:10.1016/j.ceb.2015.05.007. PMC 4522337. PMID 26079711.
  8. ↑ Liu B, Wang J, Chan KM, Tjia WM, Deng W, Guan X, Huang JD, Li KM, Chau PY, Chen DJ, Pei D, Pendas AM, Cadiñanos J, López-Otín C, Tse HF, Hutchison C, Chen J, Cao Y, Cheah KS, Tryggvason K, Zhou Z (2005). "Genomic instability in laminopathy-based premature aging". Nat. Med. 11 (7): 780–5. doi:10.1038/nm1266. PMID 15980864.

External links


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