Non B-DNA: Difference between revisions

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== Implications of Non-B DNA ==
== Implications of Non-B DNA ==
Non-B DNA can have significant implications for DNA biology and human health. For example, Z-DNA has been implicated in immunity and autoimmune diseases, such as lupus and arthritis.<ref>{{Cite journal |last=Lafer |first=E M |last2=Valle |first2=R P |last3=Möller |first3=A |last4=Nordheim |first4=A |last5=Schur |first5=P H |last6=Rich |first6=A |last7=Stollar |first7=B D |date=1983-02 |title=Z-DNA-specific antibodies in human systemic lupus erythematosus. |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC436869/ |journal=Journal of Clinical Investigation |volume=71 |issue=2 |pages=314–321 |issn=0021-9738 |pmid=6822666}}</ref> H-DNA has been implicated in genomic instability and cancer, and G-quadruplexes have been linked to telomere maintenance, oncogene activation, and cancer. Triplexes have been associated with genetic diseases, such as fragile X syndrome and Huntington's disease.
Non-B DNA can have significant implications for DNA biology and human health. For example, Z-DNA has been implicated in immunity and autoimmune diseases, such as lupus and arthritis.<ref>{{Cite journal |last=Lafer |first=E M |last2=Valle |first2=R P |last3=Möller |first3=A |last4=Nordheim |first4=A |last5=Schur |first5=P H |last6=Rich |first6=A |last7=Stollar |first7=B D |date=1983-02 |title=Z-DNA-specific antibodies in human systemic lupus erythematosus. |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC436869/ |journal=Journal of Clinical Investigation |volume=71 |issue=2 |pages=314–321 |issn=0021-9738 |pmid=6822666}}</ref> H-DNA has been implicated in genomic instability and cancer, and G-quadruplexes have been linked to telomere maintenance,<ref>{{Cite journal |last=Bryan |first=Tracy M. |date=2020-08-13 |title=G-Quadruplexes at Telomeres: Friend or Foe? |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7464828/ |journal=Molecules |volume=25 |issue=16 |pages=3686 |doi=10.3390/molecules25163686 |issn=1420-3049 |pmc=7464828 |pmid=32823549}}</ref> oncogene activation, and cancer.<ref>{{Cite journal |last=Kosiol |first=Nils |last2=Juranek |first2=Stefan |last3=Brossart |first3=Peter |last4=Heine |first4=Annkristin |last5=Paeschke |first5=Katrin |date=2021-02-25 |title=G-quadruplexes: a promising target for cancer therapy |url=https://pubmed.ncbi.nlm.nih.gov/33632214/ |journal=Molecular Cancer |volume=20 |issue=1 |pages=40 |doi=10.1186/s12943-021-01328-4 |issn=1476-4598 |pmc=7905668 |pmid=33632214}}</ref> Triplexes have been associated with genetic diseases, such as fragile X syndrome and Huntington's disease.<ref>{{Cite journal |last=Wells |first=Robert D. |date=2008-06 |title=DNA triplexes and Friedreich ataxia |url=https://onlinelibrary.wiley.com/doi/10.1096/fj.07-097857 |journal=The FASEB Journal |language=en |volume=22 |issue=6 |pages=1625–1634 |doi=10.1096/fj.07-097857 |issn=0892-6638}}</ref>

Non-B DNA structures can also affect DNA replication and transcription, leading to mutations and genome instability. In addition, non-B DNA structures can modulate chromatin structure and gene expression, affecting development, differentiation, and disease.

== Research on Non-B DNA ==
Research on non-B DNA has increased in recent years due to its potential implications in various biological processes and diseases. Studies have focused on understanding the mechanisms of non-B DNA formation, regulation, and function. For example, the role of non-B DNA structures in telomere maintenance has been studied extensively, as telomeres play a crucial role in cell aging and cancer development.

In addition, non-B DNA structures have been studied as potential targets for cancer therapy. G-quadruplexes, in particular, have been targeted by small molecules that can stabilize or destabilize these structures, leading to changes in gene expression and cell proliferation. These small molecules have shown promise in preclinical studies as potential anticancer agents.

Non-B DNA structures have also been studied as potential diagnostic tools for various diseases. For example, the detection of G-quadruplexes in circulating tumor DNA has been explored as a potential biomarker for cancer diagnosis and monitoring. Similarly, the detection of triplexes in genomic regions associated with genetic diseases has been studied as a potential diagnostic tool for these disorders.

Advances in sequencing technologies have enabled the identification and characterization of non-B DNA structures at the genomic level. High-throughput sequencing technologies, such as ChIP-seq, ATAC-seq, and Hi-C, have been used to map the distribution and regulation of non-B DNA structures in various genomic regions and cell types. These studies have revealed the complexity and diversity of non-B DNA structures and their potential roles in DNA biology and disease.


== References: ==
== References: ==

Revision as of 22:49, 26 March 2023

Non-B DNA is a term used to describe DNA conformations that differ from the canonical B-DNA conformation. B-DNA is described by James Watson and Francis Crick as the most common form of DNA found in nature,[1] but non-B DNA structures can arise due to various factors, including DNA sequence, length, supercoiling, and environmental conditions. Non-B DNA structures can have important biological roles, but they can also cause problems, such as genomic instability and disease.[2]

Types of Non-B DNA

Non-B DNA can be classified into several types, including A-DNA, Z-DNA, H-DNA, G-quadruplexes, and Triplexes (Triple-stranded DNA).

Z-DNA is a left-handed helix with a zigzag backbone, in contrast to the right-handed B-DNA helix. It is stabilized by the alternating purine-pyrimidine sequence and can form in regions of DNA with high GC-content, supercoiling, or negative superhelicity. Z-DNA has been implicated in gene regulation and immunity, but it can also induce DNA damage and inflammation.

H-DNA is a triple-stranded DNA structure that forms when two homologous DNA strands come together and one strand displaces the other. H-DNA is stabilized by Hoogsteen base pairing and can cause mutations, rearrangements, and genome instability. H-DNA is thought to be involved in DNA replication, recombination, and repair, but its precise biological functions remain unclear.

G-quadruplexes are four-stranded DNA structures formed by guanine-rich sequences. G-quadruplexes can form in telomeres, oncogene promoters, and other genomic regions and can affect gene expression, DNA replication, and telomere maintenance. G-quadruplexes are also potential targets for cancer therapy.

Triplexes are three-stranded DNA structures formed by the binding of a third strand to a DNA duplex. Triplexes can be formed by pyrimidine-rich or purine-rich third strands, and they can occur in genomic regions with inverted repeats, mirror repeats, or other special sequences. Triplexes can affect DNA replication, transcription, and recombination, but they can also cause DNA damage and mutagenesis.

Implications of Non-B DNA

Non-B DNA can have significant implications for DNA biology and human health. For example, Z-DNA has been implicated in immunity and autoimmune diseases, such as lupus and arthritis.[3] H-DNA has been implicated in genomic instability and cancer, and G-quadruplexes have been linked to telomere maintenance,[4] oncogene activation, and cancer.[5] Triplexes have been associated with genetic diseases, such as fragile X syndrome and Huntington's disease.[6]

References:

  1. ^ Richmond, Timothy J.; Davey, Curt A. (2003-05-08). "The structure of DNA in the nucleosome core". Nature. 423 (6936): 145–150. doi:10.1038/nature01595. ISSN 0028-0836. PMID 12736678.
  2. ^ Wang, Guliang; Vasquez, Karen M. (2023-04). "Dynamic alternative DNA structures in biology and disease". Nature Reviews Genetics. 24 (4): 211–234. doi:10.1038/s41576-022-00539-9. ISSN 1471-0064. {{cite journal}}: Check date values in: |date= (help)
  3. ^ Lafer, E M; Valle, R P; Möller, A; Nordheim, A; Schur, P H; Rich, A; Stollar, B D (1983-02). "Z-DNA-specific antibodies in human systemic lupus erythematosus". Journal of Clinical Investigation. 71 (2): 314–321. ISSN 0021-9738. PMID 6822666. {{cite journal}}: Check date values in: |date= (help)
  4. ^ Bryan, Tracy M. (2020-08-13). "G-Quadruplexes at Telomeres: Friend or Foe?". Molecules. 25 (16): 3686. doi:10.3390/molecules25163686. ISSN 1420-3049. PMC 7464828. PMID 32823549.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  5. ^ Kosiol, Nils; Juranek, Stefan; Brossart, Peter; Heine, Annkristin; Paeschke, Katrin (2021-02-25). "G-quadruplexes: a promising target for cancer therapy". Molecular Cancer. 20 (1): 40. doi:10.1186/s12943-021-01328-4. ISSN 1476-4598. PMC 7905668. PMID 33632214.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  6. ^ Wells, Robert D. (2008-06). "DNA triplexes and Friedreich ataxia". The FASEB Journal. 22 (6): 1625–1634. doi:10.1096/fj.07-097857. ISSN 0892-6638. {{cite journal}}: Check date values in: |date= (help)CS1 maint: unflagged free DOI (link)