Article Evaluation
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Bisulfite Sequencing
editI am evaluating the Bisulfite sequencing page.
This article is a B class and has been rated Middle Class. DNA methylation is what this treatment tests out for, and there were several links to the DNA methylation Wikipedia page as well as the individual DNA and methylation pages. A small explanation is written in the article in order to explain what bisulfite treated DNA is.
This article was thorough as it explained what different methods could’ve been used to analyze bisulfite treated DNA, but also linked the numerous methods in their own pages.
It was unnecessary to make an entire heading on Oxidative bisulfite sequencing rather than place it under the sequencing methods heading. It seemed rather biased to do that. The limitations section was overexpressed with problems and their applications.
I noticed that all facts were clearly sourced. The sources I checked were all working links and good references.
The talk page included one section, where an editor explained how he improved the article. The editor linked his edit and his page for additional information on his edits. The editor gave clear instructions on how to fix any problems he had with the URL’s or the edit itself.
The best part about this page was the talk page. The one comment shows how to improve at maximum capacity by giving other editors the chance to analyze and edit the changes as thoroughly as possible.
Edit under the subsection of Hi-C.
editResearchers attempt to study the extent of Hi-C’s detection through a study focusing on screening primary brain tumours.[1] Prior to this, Hi-C was primarily focused on cell lines.[2]
Potential Topics
editThis article is a stub article that includes basic information on the chemistry, function, and modifications.
I was hoping to update it based on N-terminus in post-translational modification and DNA. I could update the Chemistry section to talk about the structure.
This article is a stub article that has the information displayed in a very unorganized way.
I could fix the formatting of the page and add information regarding this subject that could express the significance of allelic heterogeneity in scientific literature.
This article is a stub article that also has the information displayed in an unorganized way.
It explains how in population genetics, clonal interference is significant.
I would improve this article by expanding on how it is significant in scientific literature.
The way I intend to modify this wikipedia page is by improving on the points covered. Upon looking at the page, I can see that many of the points and research I had looked into is already mentioned on the page, but rather briefly. I plan on expanding on those points, and adding an extra section to give the article an edge.
I do not view this article as a total stub, just not that well expressed. There is only so much you can do with a gene coding a transcription factor.
(I am putting x's next to anything that I have incorporated)
editTCF7L2 is located on chromosome 10q25.2-q25.3 and contains 19 exons.[3]X
TCF7L2 has an autosomal dominant inheritance type.[4]X
TCF7L2 has been shown to have a role in colorectal cancer. Upon silencing TCF7L2 in KM12 colorectal cancer cells, it was evident that TCF7L2 played a role in proliferation and metastasis of cancer cells in colorectal cancer.[5]X
Type 2 diabetes mellitus (T2DM) is a metabolic disease that is influenced by both genetic and environmental factors.[6] (Don't need it anymore)
TCF7L2 is downstream of the WNT/β-catenin pathways. The activation of the WNT/β-catenin pathway has been associated demyelination in multiple sclerosis. TCF7L2 is unregulated during early remyelination, leading scientists to believe that it is involved in remyelination. TCF7L2 could act in dependence or independent of the WNT/β-catenin pathways.[7]X
TCF7L2 is a molecular effector of the WNT/β-catenin pathways.[8]X
TCF7L2 is polymorphic.[9]
Ethnic groups may carry different T2DM risk depending on the different TCF7L2 polymorphism.[9]
T2DM susceptibility is exhibited in carriers of TCF7L2 rs7903146. The T2DM susceptibility exhibited by the polymorphism of TCF7L2 does not seem to be due to insulin resistance, but rather, seems to be due to impaired insulin secretors.[9]
TC7FL2 is expressed in pancreatic β-cells.[9]
TCF7L2 polymorphisms differ in function, making the TCF7L2 gene a pleiotropic gene. T2DM susceptibility is exhibited in carriers of TCF7L2 rs7903146C>T[6][9] and rs290481T>C[9] polymorphisms.[6][9] TCF7L2 rs290481T>C polymorphism has shown no significant correlation to the susceptibility to gestational diabetes mellitus (GDM) in a Chinese Han population, whereas the T alleles of rs7903146[9] and rs1799884[10] increase susceptibility for GDM.[9][10]
Single nucleotide polymorphisms (SNPs) in TCF7L2 have shown an increase in susceptibility to schizophrenia in Arab, European and Chinese Han associations. In the Chinese Han population, SNP rs12573128 in TCF7L2 is the variant that was associated with an increase in schizophrenia risk. It is important to note the markers associated with those diseases to use them as pre-diagnostic markers.[11]
TCF7L2’s role in glucose metabolism is expressed in many tissues such as gut, brain, liver, and skeletal muscle. However, TCF7L2 does not directly regulate glucose metabolism in β-cells, it regulates glucose metabolism in pancreatic and liver tissues.[12]
TCF7L2 modulates pancreatic islet β-cell function and is said to be significantly associated with GDM risk. [13]
TCF7L2 polymorphisms can increase susceptibility to type 2 diabetes by decreasing the production of glucagon-like peptide-1 (GLP-1).[14]
TCF7L2 is a member of the TCF family that form a bipartite transcription factor (β-catenin/TCF) alongside β-cat. Bipartite transcription factors can have large effects on the signaling Wnt signalling pathway. TCF7L2 having an effect on the Wnt signalling pathway can be demonstrated through the inhibition of Wnt signaling by the repression of TCF7L2 by HMG-box repressor HBP1.[14]
TCF7L2 is indirectly involved in prostate cancer through its role in activating the PI3K/Akt pathway.[15]
How I plan to review the Page (paragraph by paragraph):
editFirst paragraph introductory will have this added into:
editAdd a section in the beginning indicating that this is a GENE encoding a protein that acts as a transcription factor. The majority of the ways I was speaking of it indicates that it is a gene and not a transcription factor.
The TCF7L2 gene located on chromosome 10q25.2-q25.3 and contains 19 exons.[3] The TCF7L2 gene has an autosomal dominant inheritance type.[4]
Under function:
editTCF7L2 polymorphisms differ in function, making the TCF7L2 gene, encoding the transcription factor, a pleiotropic gene. TCF7L2 is the molecular effector of the WNT/β-catenin pathways.[8]
TCF7L2’s role in glucose metabolism is expressed in many tissues such as gut, brain, liver, and skeletal muscle. However, TCF7L2 does not directly regulate glucose metabolism in β-cells, it regulates glucose metabolism in pancreatic and liver tissues.[12]
Maybe you will add this under clinical significance to aid in the talk:
editT2DM susceptibility is exhibited in carriers of TCF7L2 rs7903146C>T[6][9] and rs290481T>C[9] polymorphisms.[6][9] TCF7L2 rs290481T>C polymorphism has shown no significant correlation to the susceptibility to gestational diabetes mellitus (GDM) in a Chinese Han population, whereas the T alleles of rs7903146[9] and rs1799884[10] increase susceptibility.[9][10] The difference in effects of the different polymorphisms of the gene indicate that the gene is pleiotropic.
Add gestational diabetes section in clinical significance:
editTCF7L2 modulates pancreatic islet β-cell function and is said to be significantly associated with GDM risk. [13]
Under clinical significance (cancer):
editTCF7L2 has been shown to have a role in colorectal cancer. Upon silencing TCF7L2 in KM12 colorectal cancer cells, it was evident that TCF7L2 played a role in proliferation and metastasis of cancer cells in colorectal cancer.[5]
After the part of saying it can be involved in multiple cancers:
editTCF7L2 is indirectly involved in prostate cancer through its role in activating the PI3K/Akt pathway.[15]
Add a new section in the clinical significance for Schizophrenia
editSingle nucleotide polymorphisms (SNPs) in TCF7L2 gene have shown an increase in susceptibility to schizophrenia in Arab, European and Chinese Han associations. In the Chinese Han population, SNP rs12573128 in TCF7L2 is the variant that was associated with an increase in schizophrenia risk. It is important to note the markers associated with those diseases to use them as pre-diagnostic markers.[11]
Multiple sclerosis subsection
editTCF7L2 is downstream of the WNT/β-catenin pathways. The activation of the WNT/β-catenin pathway has been associated demyelination in multiple sclerosis. TCF7L2 is unregulated during early remyelination, leading scientists to believe that it is involved in remyelination. TCF7L2 could act in dependence or independent of the WNT/β-catenin pathways.[7]
- ^ Harewood, Louise; Kishore, Kamal; Eldridge, Matthew D.; Wingett, Steven; Pearson, Danita; Schoenfelder, Stefan; Collins, V. Peter; Fraser, Peter (2017-06-27). "Hi-C as a tool for precise detection and characterisation of chromosomal rearrangements and copy number variation in human tumours". Genome Biology. 18 (1): 125. doi:10.1186/s13059-017-1253-8. ISSN 1474-760X. PMC 5488307. PMID 28655341.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Burton, Joshua N.; Adey, Andrew; Patwardhan, Rupali P.; Qiu, Ruolan; Kitzman, Jacob O.; Shendure, Jay (December 2013). "Chromosome-scale scaffolding of de novo genome assemblies based on chromatin interactions". Nature Biotechnology. 31 (12): 1119–1125. doi:10.1038/nbt.2727. ISSN 1546-1696. PMC 4117202. PMID 24185095.
- ^ a b "TCF7L2 transcription factor 7 like 2 [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2017-11-30.
- ^ a b "OMIM Entry-*602228-TRANSCRIPTION FACTOR 7-LIKE 2;TCF7L2". omim.org. Retrieved 2017-11-30.
- ^ a b Torres, Sofía; García-Palmero, Irene; Marín-Vicente, Consuelo; Bartolomé, Rubén A.; Calviño, Eva; Fernández-Aceñero, María Jesús; Casal, J. Ignacio (2017-11-21). "Proteomic Characterization of Transcription and Splicing Factors Associated with a Metastatic Phenotype in Colorectal Cancer". Journal of Proteome Research. 17 (1): 252–264. doi:10.1021/acs.jproteome.7b00548. hdl:10261/160082. ISSN 1535-3907. PMID 29131639.
- ^ a b c d e Chen, Yan; Zhao, Ying; Li, Yan-Bo; Wang, Yan-Jun; Zhang, Gui-Zhen (2018-01-01). "Detection of SNPs of T2DM susceptibility genes by a ligase detection reaction–fluorescent nanosphere technique". Analytical Biochemistry. 540–541 (Supplement C): 38–44. doi:10.1016/j.ab.2017.11.003. PMID 29128291.
- ^ a b Vallée, Alexandre; Vallée, Jean-Noël; Guillevin, Rémy; Lecarpentier, Yves (2017-09-13). "Interactions Between the Canonical WNT/Beta-Catenin Pathway and PPAR Gamma on Neuroinflammation, Demyelination, and Remyelination in Multiple Sclerosis". Cellular and Molecular Neurobiology. 38 (4): 783–795. doi:10.1007/s10571-017-0550-9. ISSN 1573-6830. PMID 28905149. S2CID 4620853.
- ^ a b Torabi, Keyvan; Wangsa, Darawalee; Ponsa, Immaculada; Brown, Markus; Bosch, Anna; Vila-Casadesús, Maria; Karpova, Tatiana S.; Calvo, Maria; Castells, Antoni (October 2017). "Transcription-dependent radial distribution of TCF7L2 regulated genes in chromosome territories". Chromosoma. 126 (5): 655–667. doi:10.1007/s00412-017-0629-6. ISSN 1432-0886. PMC 7906436. PMID 28343235.
- ^ a b c d e f g h i j k l m n Zhu, Li; Xie, Zhiqiang; Lu, Jianping; Hao, Qiu; Kang, Mingqiang; Chen, Shuchen; Tang, Weifeng; Ding, Hao; Chen, Yu (2017-08-16). "TCF7L2 rs290481 T>C polymorphism is associated with an increased risk of type 2 diabetes mellitus and fasting plasma glucose level". Oncotarget. 8 (44): 77000–77008. doi:10.18632/oncotarget.20300. ISSN 1949-2553. PMC 5652758. PMID 29100364.
- ^ a b c d Zhang, Cuilin; Bao, Wei; Rong, Ying; Yang, Huixia; Bowers, Katherine; Yeung, Edwina; Kiely, Michele (2013-05-19). "Genetic variants and the risk of gestational diabetes mellitus: a systematic review". Human Reproduction Update. 19 (4): 376–390. doi:10.1093/humupd/dmt013. ISSN 1355-4786. PMC 3682671. PMID 23690305.
- ^ a b Liu, Lijun; Li, Jingjie; Yan, Mengdan; Li, Jing; Chen, Junyu; Zhang, Yi; Zhu, Xikai; Wang, Li; Kang, Longli (2017-02-22). "TCF7L2 polymorphisms and the risk of schizophrenia in the Chinese Han population". Oncotarget. 8 (17): 28614–28620. doi:10.18632/oncotarget.15603. ISSN 1949-2553. PMC 5438676. PMID 28404897.
- ^ a b Facchinello, Nicola; Tarifeño-Saldivia, Estefania; Grisan, Enrico; Schiavone, Marco; Peron, Margherita; Mongera, Alessandro; Ek, Olivier; Schmitner, Nicole; Meyer, Dirk (2017-08-29). "Tcf7l2 plays pleiotropic roles in the control of glucose homeostasis, pancreas morphology, vascularization and regeneration". Scientific Reports. 7 (1): 9605. doi:10.1038/s41598-017-09867-x. ISSN 2045-2322. PMC 5575064. PMID 28851992.
- ^ a b Zhang, Cuilin; Bao, Wei; Rong, Ying; Yang, Huixia; Bowers, Katherine; Yeung, Edwina; Kiely, Michele (July 2013). "Genetic variants and the risk of gestational diabetes mellitus: a systematic review". Human Reproduction Update. 19 (4): 376–390. doi:10.1093/humupd/dmt013. ISSN 1460-2369. PMC 3682671. PMID 23690305.
- ^ a b Jin, Tianru; Liu, Ling (November 2008). "The Wnt signaling pathway effector TCF7L2 and type 2 diabetes mellitus". Molecular Endocrinology (Baltimore, Md.). 22 (11): 2383–2392. doi:10.1210/me.2008-0135. ISSN 0888-8809. PMID 18599616.
- ^ a b Sun, Ping; Xiong, Hui; Kim, Tae Hoon; Ren, Bing; Zhang, Zhuohua (2006-02-01). "Positive Inter-Regulation between β-Catenin/T Cell Factor-4 Signaling and Endothelin-1 Signaling Potentiates Proliferation and Survival of Prostate Cancer Cells". Molecular Pharmacology. 69 (2): 520–531. doi:10.1124/mol.105.019620. ISSN 0026-895X. PMID 16291872. S2CID 10148857.