User:Davidschrampr/sandbox
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Article evaluation[edit]
TATA-binding protein
The article includes information that is relevant to the topic and does not include unnecessary information. The article includes diagrams and graphics that help the reader visualize and understand structure, location and function. However, the article appears to be missing some important research information. The article is mostly neutral but does include speculation and assumptions based on data and experiments that have not been verified yet. The links provided for citations are clickable and lead to the original article. The sources directly support the information provide in the article. The information from the citations are found in reliable primary journal articles. No bias is present in the source journals. The article seems to be somewhat incomplete in terms of structure of the TATA-binding protein. The article seems up to date and includes papers from September 2017. Currently no discussion about the article are being had on the Talk page. The rating on the article is B-Class and is part of the WIkiProject Genetics and the WikiProject Molecular and Cell Biology projects.
Good job. Keep it up! AdamCF87 (talk) 17:42, 5 October 2017 (UTC)
Adding to an Article[edit]
Added 2 sentences to the poison dart frog article.
Poison dart frogs containing epibatidine have undergone a 3 amino acid mutation on receptors of the body, allowing the frog to be resistant to its own poison. Epibatidine-producing frogs have evolved poison resistance of body receptors independently three times.
Possible Edits[edit]
-include description of structure, chromosomal location, effects of upregulation and downregulation, links to cancer, other important elements, affects on transcription and types of cancer associated and prognosis for each type.
Sources:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3377072/
https://www.ncbi.nlm.nih.gov/pubmed/21328542
https://www.ncbi.nlm.nih.gov/pubmed/27650486
https://www.ncbi.nlm.nih.gov/pubmed/25742952
https://link.springer.com/article/10.1007/s13258-017-0577-9
https://www.ncbi.nlm.nih.gov/pubmed/21337521
http://cancerres.aacrjournals.org/content/75/15_Supplement/3929
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5342799/
https://bmcdevbiol.biomedcentral.com/articles/10.1186/1471-213X-8-108
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799278/
https://doaj.org/article/95ca9e07eb494a3daaa91588e25659bc
Article Draft[edit]
ZNF703[edit]
From Wikipedia, the free encylopedia
The zinc finger protein 703 (ZNF703) gene is an oncogene commonly associated with luminal B breast cancer.[1] ZNF703 is contained within the NET/N1z family responsible for regulation of transcription essential for developmental growth especially in the hindbrain.[1] Normal functions performed by ZNF703 include adhesion, movement and proliferation of cells.[1] ZNF703 directly accumulates histone deacetylases at gene promoter regions but does not bind to functional DNA.[2]
Discovery of ZNF703 by researchers at the Cancer Research UK charity marks the first new oncogene detected within the last 6 years.[1]
ZNF703 can be located on chromosome 8 on the telomeric amplicon region 8p12 in humans.[3]
Patients diagnosed with luminal B cancer caused by ZNF703 typically have lower recovery and survival rates than other cancer types.[4]
Drug resistance of ZNF703 has been displayed when patients are treated using anti-cancer drug Tamoxifen.[5]
Discovery[edit]
Researchers discovered the carcinogenic nature of ZNF703 in 2011 while conducting research on the classification and resistance of various oncogenes.[1] Researchers attempted to discern factors associated with various cancer types through observation of oncogenic mechanism on a molecular scale.[1] The luminal B cancer pathway exhibited an amplification of 5 different genomic areas including the chromosome region 8p12.[1] Amplification of region 8p12 occured through transcriptional regulation of ZNF703.[1]
Location[edit]
ZNF703 is located on human chromosome 8 at the short arm region commonly named chromosome region 8p12.[3] The gene spans 590 base pairs long with a transcript of 2978 base pairs.[6] Tumors generated by ZNF703 have shown loss in size beginning at the telomere and ending at 8p12 while the 8p12-11 region has increased size.[6] A fluctuation between increase and decrease is present along the 8p12-8p21 boundary region of the chromosome.[6] A pattern has been found that involves three similar regions of disrupted growth and 4 regions of enhanced growth starting from the telomere and ending at the centromere.[6]
Role in Cancer[edit]
The ZNF703 gene generally plays an active role in luminal B tumor cells contained in mammary ducts.[3] Typically, ZNF703 expression is greater when the tumors are estrogen receptor positive as opposed to estrogen receptor negative.[3] ZNF703 is co-expressed in a nuclear complex containing genes DCAF7, NCRO2 and PHB2.[3] ZNF703 generates a nuclear protein responsible for oestrogen receptor associated protein repression.[3] Gene expression of stem cells are triggered when the ZNF703 gene becomes overexpressed in the complex.[3] As a result, both regular cells and cancer stem cell abundance increases rapidly.[3] ZNF703 overexpression also causes primary and secondary tumorsphere development alongside amplified production of CD49F- positive cells associated with colon cancer.[3]
ZNF703 also experiences target regulation of cancer cells through the transcription of RNA SPRY4-It1.[7] RNA SPRY4-IT1 is a non-coding gene responsible for preventing apoptosis and generating larger tumors.[7]
Researchers recently established a link between the trigger gene ZNF703 and Akt/mTOR pathway activation involved in the cellular cycle resulting in lung tumor formation.[8]
Prognosis[edit]
The lifespan of individuals with colorectal cancer and luminal cancer have different prognosis depending on the amount of expression of the ZNF703 gene.[4] Low amounts of transcription of ZNF703 usually leads to a healthier prognosis than individuals experiencing higher levels of transcription of the oncogene.[4] ZNF703 is a target for therapeutic medicines since survival rates increase as transcription rates decrease.[4]
Resistance to drugs[edit]
The drug Tamoxifen is a commonly administered drug used to treat luminal cancers in patients.[5] Half of patients treated with Tamoxifen are resistant to the drug.[5] Overexpression of ZNF703 has been linked to Tamoxifen resistance.[5] As transcription of the ZNF703 gene reaches substantial levels, instead of blocking cell proliferation, Tamoxifen is found to increase cancer cell division.[5] Tamoxifen can only be given at low dosages and patients are monitored daily in order to avoid tumor growth.[5]
References[edit]
- ^ a b c d e f g h Yang, Gongli; Ma, Feng; Zhong, Muxiao; Fang, Lin; Peng, Yao; Xin, Xiaoming; Zhong, Jietao; Yuan, Fangfang; Gu, Hongxiang; Zhu, Wei; Zhang, Yali (2011). "ZNF703 acts as an oncogene that promotes progression in gastric cancer". Oncology Reports: 1877-1882. doi:https://doi.org/10.3892/or.2014.2997.
{{cite journal}}:|access-date=requires|url=(help); Check|doi=value (help); External link in|doi= - ^ Nakamura, Mako; Choe, Seong-Kyu; Runko, Alexander P; Gardner, Paul D; Sagerstrom, Charles G (2008). "Nlz1/Znf703 acts as a repressor of transcription". BMC Developmental Biology. 8. doi:https://doi.org/10.1186/1471-213X-8-108.
{{cite journal}}:|access-date=requires|url=(help); Check|doi=value (help); External link in|doi= - ^ a b c d e f g h i Sircoulomb, Fabrice; Nicolas, Nathalie; Ferrari, Anthony; Finetti, Pascal; Bekhouche, Ismahane; Rousselet, Estelle; Lonigro, Aurelie; Adelaide, Jose; Baudelet, Emilie; Esteyries, Severine; Wicinksi, Julien; Audebert, Stephane; Charade-Jauffret, Emmanuelle; Jacquemier, Jocelyne; Lopez, Marc; Borg, Jean-Paul; Sotiriou, Christos; Popovici, Cornel; Bertucci, Fancois; Birnbaum, Daniel; Chaffanet, Max; Ginestier, Christophe (2011). "ZNF703 gene amplification at 8p12 specifies luminal B breast cancer". EMBO Molecular Medicine. 3 (3): 153–166. doi:10.1002/emmm.201100121.
{{cite journal}}:|access-date=requires|url=(help) - ^ a b c d Ma, Feng; Bi, Lihong; Yang, Gongli; Zhang, Mengnan; Liu, Cuiping; Zhao, Yingying; Wang, Yadong; Wang, Jide; Bai, Yang; Zhang, Yali (2014). "ZNF703 promotes tumor cell proliferation and invasion and predicts poor prognosis in patients with colorectal cancer". Oncology Reports. 32: 1071-1077. doi:10.3892/or.2014.3313.
{{cite journal}}:|access-date=requires|url=(help) - ^ a b c d e f Zhang, Xi; Mu, Xin; Huang, Ou; Xie, Zuoquan; Jiang, Min; Geng, Meiyu; Shen, Kunwei (2013). "Luminal Breast Cancer Cell Lines Overexpressing ZNF703 Are Resistant to Tamoxifen through Activation of Akt/ mTOR Signaling". PloS one. 8 (8). doi:10.1371/journal.pone.0072053.
{{cite journal}}:|access-date=requires|url=(help)CS1 maint: unflagged free DOI (link) - ^ a b c d Gelsi-Boyer, Veronique; Orsetti, Beatrice; Cervera, Nathalie; Finetti, Pascal; Sircoulomb, Fabrice; Rouge, Carole; Lasorsa, Laurence; Letessier, Anne; Ginestier, Christophe; Monville, Florence; Esteyries, Severine; Jose, Adelaide; Esterni, Benjamin; Henry, Catherine; Ethier, Stephen P; Bibeau, Frederic; Mozziconacci, Marie-Joelle; Charafe-Jauffret, Emmanuelle; Jacquemier, Jocelyne; Bertucci, Francois; Birnbaum, Daniel; Theillet, Charles; Chaffanet, Max (2005). "Comprehensive Profiling of 8p11-12 Amplification in Breast Cancer". Molecular Cancer Research. 3 (12). doi:10.1158/1541-7786.MCR-05-0128.
{{cite journal}}:|access-date=requires|url=(help) - ^ a b Shi, Yongguo; Li, Juan; Liu, Yangchen; DIng, Jie; Fan, Yingrui; Yun, Tian; Wang, Li; Lian, Yifan; Wang, Keming; Shu, Yongqian (2015). "The long noncoding RNA SPRY4-IT1 increases the proliferation of human breast cancer cells by upregulating ZNF703 expression". Molecular Cancer. 14 (51). doi:10.1186/s12943-015-0318-0.
{{cite journal}}:|access-date=requires|url=(help)CS1 maint: unflagged free DOI (link) - ^ Baykara, Onur; Dalay, Nejat; Kaynak, Kamil; Buyru, Nur (2016). "ZNF703 Overexpression may act as an oncogene in non-small cell lung cancer". Cancer Medicine. 5 (10): 2873-2878. doi:10.1002/cam4.847.
{{cite journal}}:|access-date=requires|url=(help)