SOD1

SOD1
ساختارهای موجود
PDBجستجوی هم‌ساخت‌شناسی: PDBe RCSB
معین‌کننده‌ها
نام‌های دیگرSOD1, ALS, ALS1, HEL-S-44, IPOA, SOD, hSod1, homodimer, superoxide dismutase 1, soluble, superoxide dismutase 1, STAHP
شناسه‌های بیرونیOMIM: 147450; MGI: 98351; HomoloGene: 392; GeneCards: SOD1; OMA:SOD1 - orthologs
عدد EC1.15.1.1
هم‌ساخت‌شناسی
گونه‌هاانسانموش
Entrez

6647

20655

Ensembl

ENSG00000142168

ENSMUSG00000022982

UniProt

P00441

P08228

RefSeq (mRNA)

NM_000454

NM_011434

RefSeq (پروتئین)

NP_000445

NP_035564

موقعیت (UCSC)Chr 21: 31.66 – 31.67 MbChr 16: 90.02 – 90.02 Mb
جستجوی PubMed[۳][۴]
ویکی‌داده
مشاهده/ویرایش انسانمشاهده/ویرایش موش

سوپراکسید دیسموتاز ۱ (انگلیسی: SOD1) یک آنزیم است که در انسان توسط ژن «SOD1» (بر روی کروموزوم ۲۱) کدگذاری می‌شود. SOD1 یکی از انواع سه‌گانهٔ سوپراکسید دیسموتاز است.[۵][۶]

اهمیت این آنزیم در آن است که در آپوپتوز و در بروز بیماری اسکلروز جانبی آمیوتروفیک (ALS)[۶] (انواع ارثی[۷][۸][۹] یا تک‌گیر[۱۰] آن) نقش دارد.

منابع

  1. ↑ ۱٫۰ ۱٫۱ ۱٫۲ GRCh38: Ensembl release 89: ENSG00000142168 – Ensembl, May 2017
  2. ↑ ۲٫۰ ۲٫۱ ۲٫۲ GRCm38: Ensembl release 89: ENSMUSG00000022982 – Ensembl, May 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.
  5. ↑ Milani P, Gagliardi S, Cova E, Cereda C (2011). "SOD1 Transcriptional and Posttranscriptional Regulation and Its Potential Implications in ALS". Neurology Research International. 2011: 458427. doi:10.1155/2011/458427. PMC 3096450. PMID 21603028.{{cite journal}}: نگهداری یادکرد:doi رایگان بی‌نشان (رده) نگهداری یادکرد:شماره مقاله به‌جای شماره صفحه (رده)
  6. ↑ ۶٫۰ ۶٫۱ Rosen DR, Siddique T, Patterson D, Figlewicz DA, Sapp P, Hentati A, Donaldson D, Goto J, O'Regan JP, Deng HX (March 1993). "Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis". Nature. 362 (6415): 59–62. Bibcode:1993Natur.362...59R. doi:10.1038/362059a0. PMID 8446170.
  7. ↑ Conwit RA (December 2006). "Preventing familial ALS: a clinical trial may be feasible but is an efficacy trial warranted?". Journal of the Neurological Sciences. 251 (1–2): 1–2. doi:10.1016/j.jns.2006.07.009. PMID 17070848.
  8. ↑ Al-Chalabi A, Leigh PN (August 2000). "Recent advances in amyotrophic lateral sclerosis". Current Opinion in Neurology. 13 (4): 397–405. doi:10.1097/00019052-200008000-00006. PMID 10970056.
  9. ↑ Redler RL, Dokholyan NV (2012-01-01). "The complex molecular biology of amyotrophic lateral sclerosis (ALS)". Progress in Molecular Biology and Translational Science. Progress in Molecular Biology and Translational Science. 107: 215–62. doi:10.1016/B978-0-12-385883-2.00002-3. ISBN 9780123858832. PMC 3605887. PMID 22482452.
  10. ↑ Gagliardi S, Cova E, Davin A, Guareschi S, Abel K, Alvisi E, Laforenza U, Ghidoni R, Cashman JR, Ceroni M, Cereda C (August 2010). "SOD1 mRNA expression in sporadic amyotrophic lateral sclerosis". Neurobiology of Disease. 39 (2): 198–203. doi:10.1016/j.nbd.2010.04.008. PMID 20399857.

بیشتر بخوانید

  • de Belleroche J, Orrell R, King A (November 1995). "Familial amyotrophic lateral sclerosis/motor neurone disease (FALS): a review of current developments". Journal of Medical Genetics. 32 (11): 841–7. doi:10.1136/jmg.32.11.841. PMC 1051731. PMID 8592323.
  • Ceroni M, Curti D, Alimonti D (2002). "Amyotrophic lateral sclerosis and SOD1 gene: an overview". Functional Neurology. 16 (4 Suppl): 171–80. PMID 11996514.
  • Zelko IN, Mariani TJ, Folz RJ (August 2002). "Superoxide dismutase multigene family: a comparison of the CuZn-SOD (SOD1), Mn-SOD (SOD2), and EC-SOD (SOD3) gene structures, evolution, and expression". Free Radical Biology & Medicine. 33 (3): 337–49. doi:10.1016/S0891-5849(02)00905-X. PMID 12126755.
  • Hadano S (June 2002). "[Causative genes for familial amyotrophic lateral sclerosis]". Seikagaku. the Journal of Japanese Biochemical Society. 74 (6): 483–9. PMID 12138710.
  • Noor R, Mittal S, Iqbal J (September 2002). "Superoxide dismutase--applications and relevance to human diseases". Medical Science Monitor. 8 (9): RA210–5. PMID 12218958.
  • Potter SZ, Valentine JS (April 2003). "The perplexing role of copper-zinc superoxide dismutase in amyotrophic lateral sclerosis (Lou Gehrig's disease)". Journal of Biological Inorganic Chemistry. 8 (4): 373–80. doi:10.1007/s00775-003-0447-6 (inactive 2017-01-24). PMID 12644909.{{cite journal}}: نگهداری یادکرد:doi غیرفعال از ژانویه 2017 (رده)
  • Rotilio G, Aquilano K, Ciriolo MR (2004). "Interplay of Cu,Zn superoxide dismutase and nitric oxide synthase in neurodegenerative processes". IUBMB Life. 55 (10–11): 629–34. doi:10.1080/15216540310001628717. PMID 14711010.
  • Jafari-Schluep HF, Khoris J, Mayeux-Portas V, Hand C, Rouleau G, Camu W (January 2004). "[Superoxyde dismutase 1 gene abnormalities in familial amyotrophic lateral sclerosis: phenotype/genotype correlations. The French experience and review of the literature]". Revue Neurologique. 160 (1): 44–50. PMID 14978393.
  • Faraci FM, Didion SP (August 2004). "Vascular protection: superoxide dismutase isoforms in the vessel wall". Arteriosclerosis, Thrombosis, and Vascular Biology. 24 (8): 1367–73. doi:10.1161/01.ATV.0000133604.20182.cf. PMID 15166009.
  • Gagliardi S, Ogliari P, Davin A, Corato M, Cova E, Abel K, Cashman JR, Ceroni M, Cereda C (August 2011). "Flavin-containing monooxygenase mRNA levels are up-regulated in als brain areas in SOD1-mutant mice". Neurotoxicity Research. 20 (2): 150–8. doi:10.1007/s12640-010-9230-y. PMID 21082301.
  • Battistini S, Ricci C, Lotti EM, Benigni M, Gagliardi S, Zucco R, Bondavalli M, Marcello N, Ceroni M, Cereda C (June 2010). "Severe familial ALS with a novel exon 4 mutation (L106F) in the SOD1 gene". Journal of the Neurological Sciences. 293 (1–2): 112–5. doi:10.1016/j.jns.2010.03.009. PMID 20385392.
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