فَرْطُ كوليسترول الدَّم العائِلِيّ*[1]

ملاحظات

عدل
  • ^ أو فَرْطُ كوليستيرول الدَّم العائِلِيّ أو فَرْطُ كولِسترول الدَّم العائِلِيّ.

المراجع

عدل
  1. ^ "ترجمةُ (Familial hypercholesterolemia) في المعجم الطبي الموحد". مكتبة لبنان ناشرون. اطلع عليه بتاريخ 2018-06-18.
Major pathways of DNA repair and one tolerance mechanism
Repair pathway Lesions Accuracy Ref.
ترميم استئصال القاعدة corrects DNA damage from oxidation, deamination and alkylation, also single-strand breaks accurate [1][2]
ترميم استئصال النوكليوتيد oxidative endogenous lesions such as cyclopurine, sunlight induced thymine dimers (cyclobutane dimers and pyrimidine (6-4) pyrimidone photoproducts) accurate [3][4][5]
Homologous recombinational repair double-strand breaks in the mid-طور التركيب or mid-طور النمو الثاني of the cell cycle accurate [6]
Non-homologous end joining double-strand breaks if cells are in the G0 phase. the طور النمو الأول or the طور النمو الثاني of the cell cycle somewhat inaccurate [6]
Microhomology-mediated end joining or alt-End joining double-strand breaks in the طور التركيب of the cell cycle always inaccurate [6]
ترميم الدنا غير المتطابق base substitution mismatches and insertion-deletion mismatches generated during DNA replication accurate [7]
Direct reversal (MGMT amd AlkB) 6-O-methylguanine is reversed to guanine by MGMT, some other methylated bases are demethylated by AlkB accurate [8]
Translesion synthesis DNA damage tolerance process that allows the DNA replication machinery to replicate past DNA lesions may be inaccurate [9]
  1. ^ Krokan HE، Bjørås M (أبريل 2013). "Base excision repair". Cold Spring Harb Perspect Biol. ج. 5 ع. 4: a012583. DOI:10.1101/cshperspect.a012583. PMC:3683898. PMID:23545420.
  2. ^ del Rivero J، Kohn EC (أبريل 2017). "PARP Inhibitors: The Cornerstone of DNA Repair-Targeted Therapies". Oncology (Williston Park, N.Y.). ج. 31 ع. 4: 265–73. PMID:28412778.
  3. ^ Schärer OD (أكتوبر 2013). "Nucleotide excision repair in eukaryotes". Cold Spring Harb Perspect Biol. ج. 5 ع. 10: a012609. DOI:10.1101/cshperspect.a012609. PMC:3783044. PMID:24086042.
  4. ^ de Boer J، Hoeijmakers JH (مارس 2000). "Nucleotide excision repair and human syndromes". Carcinogenesis. ج. 21 ع. 3: 453–60. DOI:10.1093/carcin/21.3.453. PMID:10688865.
  5. ^ Satoh MS، Jones CJ، Wood RD، Lindahl T (يوليو 1993). "DNA excision-repair defect of xeroderma pigmentosum prevents removal of a class of oxygen free radical-induced base lesions". Proc. Natl. Acad. Sci. U.S.A. ج. 90 ع. 13: 6335–9. DOI:10.1073/pnas.90.13.6335. PMC:46923. PMID:8327515.
  6. ^ أ ب ت Ceccaldi R، Rondinelli B، D'Andrea AD (يناير 2016). "Repair Pathway Choices and Consequences at the Double-Strand Break". Trends Cell Biol. ج. 26 ع. 1: 52–64. DOI:10.1016/j.tcb.2015.07.009. PMC:4862604. PMID:26437586.
  7. ^ Kunkel TA، Erie DA (2005). "DNA mismatch repair". Annu. Rev. Biochem. ج. 74: 681–710. DOI:10.1146/annurev.biochem.74.082803.133243. PMID:15952900.
  8. ^ Yi C، He C (يناير 2013). "DNA repair by reversal of DNA damage". Cold Spring Harb Perspect Biol. ج. 5 ع. 1: a012575. DOI:10.1101/cshperspect.a012575. PMC:3579392. PMID:23284047.
  9. ^ Lehmann AR (2004). "Replication of damaged DNA by translesion synthesis in human cells". FEBS Letters. ج. 579 ع. 4: 873–876. DOI:10.1016/j.febslet.2004.11.029.