Gene project: Difference between revisions
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# Examples added: [[ACTR1B]], [[SVIL]], [[PHEX]], [[TFIIA]], [[STC1]], [[STC2]], [[SLC34A3]], [[E2F4]], [[HBB]], [[HBA1]] same as [[Hemoglobin, alpha 1]], [[CST1]], [[CST2]], [[ZSCAN22]] and [[Small nucleolar RNA SNORD115]]. | # Examples added: [[ACTR1B]], [[SVIL]], [[PHEX]], [[TFIIA]], [[STC1]], [[STC2]], [[SLC34A3]], [[E2F4]], [[HBB]], [[HBA1]] same as [[Hemoglobin, alpha 1]], [[CST1]], [[CST2]], [[ZSCAN22]] and [[Small nucleolar RNA SNORD115]]. | ||
# Needed include [[ZSCAN4]] that are on Wikipedia. | # Needed include [[ZSCAN4]] that are on Wikipedia. | ||
==Complement copies== | |||
{{main|Complement copy gene transcriptions}} | |||
==Inverse copies== | |||
{{main|Inverse copy gene transcriptions}} | |||
For "AGC, one copy in inverse orientation of the AGC box (AGCCGCC) [is] present as two copies (-1346 and -1314) in the ERE".<ref name=Metzger>{{ cite journal | |||
|author=Gerhard Leubner-Metzger, Luciana Petruzzelli, Rosa Waldvogel, Regina Vögeli-Lange, and Frederick Meins, Jr. | |||
|title=Ethylene-responsive element binding protein (EREBP) expression and the transcriptional regulation of class I β-1, 3-glucanase during tobacco seed germination | |||
|journal=Plant Molecular Biology | |||
|date=November 1998 | |||
|volume=38 | |||
|issue=5 | |||
|pages=785-95 | |||
|url=http://link.springer.com/article/10.1023/A:1006040425383 | |||
|arxiv= | |||
|bibcode= | |||
|doi=10.1023/A:1006040425383 | |||
|pmid= | |||
|accessdate=2014-05-02 }}</ref> | |||
==Complement-inverse copies== | |||
{{main|Complement-inverse copy gene transcriptions}} | |||
==Methylation== | |||
{{main|Methylation gene transcriptions|Methylations}} | |||
"Cytosines in CpG dinucleotides can be methylated to form 5-methylcytosine. In mammals, methylating the cytosine within a gene can turn the gene off, a mechanism that is part of a larger field of science studying gene regulation that is called epigenetics. Enzymes that add a methyl group are called DNA methyltransferases."<ref name=CpGSite>{{ cite web | |||
|title=CpG site | |||
|publisher=Wikimedia Foundation, Inc | |||
|location=San Francisco, California | |||
|date=January 30, 2013 | |||
|url=http://en.wikipedia.org/wiki/CpG_site | |||
|accessdate=2013-02-07 }}</ref> | |||
In mammals, 70% to 80% of CpG cytosines are methylated.<ref name="Jabbari2004">{{ cite journal | |||
|author=Jabbari K, Bernardi G | |||
|title=Cytosine methylation and CpG, TpG (CpA) and TpA frequencies | |||
|journal=Gene | |||
|volume=333 | |||
|issue= | |||
|pages=143–9 | |||
|date=May 2004 | |||
|pmid=15177689 | |||
|doi=10.1016/j.gene.2004.02.043 | |||
|url=http://linkinghub.elsevier.com/retrieve/pii/S0378111904000836 }}</ref> | |||
"CpG dinucleotides have long been observed to occur with a much lower frequency in the sequence of vertebrate genomes than would be expected due to random chance. For example, in the human genome, which has a 42% GC content, a pair of nucleotides consisting of cytosine followed by guanine would be expected to occur 0.21 * 0.21 = 4.41% of the time. The frequency of CpG dinucleotides in human genomes is 1% — less than one-quarter of the expected frequency."<ref name=CpGSite/> | |||
Unmethylated CpG sites can be detected by Toll-Like Receptor 9<ref name=Ramirez>{{ cite journal | |||
|author=Ramirez-Ortiz ZG, Specht CA, Wang JP, Lee CK, Bartholomeu DC, Gazzinelli RT, Levitz SM | |||
|title=Toll-like receptor 9-dependent immune activation by unmethylated CpG motifs in Aspergillus fumigatus DNA | |||
|journal=Infect Immun. | |||
|date=2008 | |||
|volume=76 | |||
|issue=5 | |||
|pages=2123–9 | |||
|pmid=18332208 | |||
|doi=10.1128/IAI.00047-08 }}</ref> "(TLR 9) on plasmacytoid dendritic cells and B cells in humans. This is used to detect intracellular viral, fungal, and bacterial pathogen DNA."<ref name=CpGSite/> | |||
Methylation is central to imprinting, along with histone modifications.<ref name="Feil2007">{{ cite journal | |||
|author=Feil R, Berger F | |||
|title=Convergent evolution of genomic imprinting in plants and mammals | |||
|journal=Trends Genet | |||
|volume=23 | |||
|issue=4 | |||
|pages=192–9 | |||
|date=2007 | |||
|pmid=17316885 | |||
|doi=10.1016/j.tig.2007.02.004 }}</ref> Most of the methylation occurs a short distance from the CpG islands (at "CpG island shores") rather than in the islands themselves.<ref name=Irizarry>{{ cite journal | |||
| author=Irizarry RA, Ladd-Acosta C, Wen B, Wu Z, Montano C, Onyango P, Cui H, Gabo K, Rongione M, Webster M, Ji H, Potash JB, Sabunciyan S, Feinberg AP | |||
| title=The human colon cancer methylome shows similar hypo- and hypermethylation at conserved tissue-specific CpG island shores | |||
| journal=Nature Genetics | |||
| volume=41 | |||
| issue=2 | |||
| date=2009 | |||
| pages=178-86 | |||
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729128/ | |||
| pmid=19151715 }}</ref> | |||
Methylation of CpG sites within the promoters of genes can lead to their silencing, a feature found in a number of human cancers (for example the silencing of tumor suppressor genes). In contrast, the hypomethylation of CpG sites has been associated with the over-expression of oncogenes within cancer cells.<ref name="Jones1999">{{ cite journal | |||
|author=Jones PA, Laird PW | |||
|title=Cancer epigenetics comes of age | |||
|journal=Nat. Genet. | |||
|volume=21 | |||
|issue=2 | |||
|pages=163–7 | |||
|date=February 1999 | |||
|pmid=9988266 | |||
|doi=10.1038/5947 }}</ref> | |||
"In eukaryotes, CpG methylation is an epigenetic DNA modification that is important for heterochromatin formation."<ref name=Tanaka>{{ cite journal | |||
|author=Yoshinori Tanaka, Hitoshi Kurumizaka, and Shigeyuki Yokoyama | |||
|title=CpG methylation of the CENP-B box reduces human CENP-B binding | |||
|journal=The FEBS Journal | |||
|month=January | |||
|year=2005 | |||
|volume=272 | |||
|issue=1 | |||
|pages=282–289 | |||
|url=http://onlinelibrary.wiley.com/doi/10.1111/j.1432-1033.2004.04406.x/full | |||
|arxiv= | |||
|bibcode= | |||
|doi=10.1111/j.1432-1033.2004.04406.x | |||
|pmid=15634350 | |||
|accessdate=2017-02-05 }}</ref> | |||
"CENP-B preferentially binds to the unmethylated CENP-B box DNA."<ref name=Tanaka/> | |||
The "CpG methylations of the CENP-B box sequence may function in [RNA interference (RNAi)] RNAi-dependent heterochromatin formation by regulating CENP-B-binding to the CENP-B box sequence in the α-satellite repeats."<ref name=Tanaka/> | |||
==Deamination== | |||
{{main|Deamination gene trancriptions|Deaminations}} | |||
The CpG deficiency is due to an increased vulnerability of methylcytosines to spontaneously deaminate to thymine in genomes with CpG cytosine methylation.<ref name=Scarano>{{ cite journal | |||
|author=Scarano E, Iaccarino M, Grippo P, Parisi E | |||
|title=The heterogeneity of thymine methyl group origin in DNA pyrimidine isostichs of developing sea urchin embryos | |||
|journal=Proceedings of the National Academy of Sciences USA | |||
|volume=57 | |||
|issue=5 | |||
|pages=1394–400 | |||
|date=1967 | |||
|pmid=5231746 | |||
|doi=10.1073/pnas.57.5.1394 | |||
|pmc=224485 }}</ref> | |||
==Ubiquitination== | |||
{{main|Ubiquitination gene trancriptions|Ubiquitinations}} | |||
==Phosphorylation== | |||
{{main|Phosphorylation gene trancriptions|Phosphorylations}} | |||
==Acknowledgements== | |||
The content on this page was first contributed by: Henry A. Hoff. | |||
==See also== | |||
{{div col|colwidth=20em}} | |||
* [[A1BG gene transcription core promoters]] | |||
* [[A1BG gene transcriptions]] | |||
* [[A1BG regulatory elements and regions]] | |||
* [[A1BG response element negative results]] | |||
* [[A1BG response element positive results]] | |||
* [[Complex locus A1BG and ZNF497]] | |||
{{Div col end}} | |||
==References== | |||
{{reflist|2}} | |||
==External links== | |||
* [http://www.genome.jp/ GenomeNet KEGG database] | |||
* [http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene Home - Gene - NCBI] | |||
* [http://www.ncbi.nlm.nih.gov/sites/gquery NCBI All Databases Search] | |||
* [http://www.ncbi.nlm.nih.gov/ncbisearch/ NCBI Site Search] | |||
* [http://www.ncbi.nlm.nih.gov/pccompound PubChem Public Chemical Database] | |||
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{{Gene project}} | |||
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[[Category:Resources last modified in January 2021]] | |||
Latest revision as of 05:28, 4 January 2021
Each of the gene infoboxes on WikiDoc display "VALUE_ERROR (nil)" at the top instead of the gene name followed by answers obtained from WikiData for each entry.
Compare ZSCAN21 on WikiDoc with ZSCAN21 on Wikipedia.
Source of the Error
The {{Infobox_gene}} template calls Module:Infobox gene which in turn calls WikiData using local ref_url = "https://www.wikidata.org/wiki/".
The reason none of the gene inboxes work is that Module:Infobox gene here is the same as Module:Infobox gene on Wikiversity or Wikipedia which both work. In short, WikiDoc is outside the WikiData WMF project computers.
Solutions
In order to produce functional gene Infoboxes the Module:Infobox gene needs to be re-programmed to call the original sources of the information to have it appropriately displayed.
Some changes along these lines have been introduced into the Infobox gene for Alpha-1-B glycoprotein, which is of interest to me. Constructing the Species Human Mouse table for inclusion has hit a template snag here on WikiDoc.
Not on Wikipedia or WikiData
Wikipedia and WikiData do not cover all known human genes that are likely of interest to WikiDoc. Examples include ZSCAN22, ZIM2, ZNF17, ZNF132, ZNF134, ZNF135, ZNF154, ZNF256, ZNF211, TRAPPC2B, ZNF460, ZNF324, ZNF544, ZNF586, ZNF444, ZNF416, ZNF446, ZNF304, USP29, ZNF667, ZSCAN18, ZSCAN5A, ZNF329, ZNF419, ZNF552, ZNF671, ZNF606, ZBTB45, ZNF587, GALP, ZNF551, ZNF835, ZIM3, ZNF837, ZNF543, ZNF787, SMIM17, ZNF418, ZNF417, ZNF548, ZNF582, ZNF583, ZNF550, ZNF584, ZNF549, ZNF547, ZIK1, ZNF776, ZSCAN1, ZSCAN5B, ZNF530, ZNF773, ZNF582-AS1, ZNF470 and MIR6806.
Needed on WikiDoc
- Examples added: ACTR1B, SVIL, PHEX, TFIIA, STC1, STC2, SLC34A3, E2F4, HBB, HBA1 same as Hemoglobin, alpha 1, CST1, CST2, ZSCAN22 and Small nucleolar RNA SNORD115.
- Needed include ZSCAN4 that are on Wikipedia.
Complement copies
Inverse copies
For "AGC, one copy in inverse orientation of the AGC box (AGCCGCC) [is] present as two copies (-1346 and -1314) in the ERE".[1]
Complement-inverse copies
Methylation
"Cytosines in CpG dinucleotides can be methylated to form 5-methylcytosine. In mammals, methylating the cytosine within a gene can turn the gene off, a mechanism that is part of a larger field of science studying gene regulation that is called epigenetics. Enzymes that add a methyl group are called DNA methyltransferases."[2]
In mammals, 70% to 80% of CpG cytosines are methylated.[3]
"CpG dinucleotides have long been observed to occur with a much lower frequency in the sequence of vertebrate genomes than would be expected due to random chance. For example, in the human genome, which has a 42% GC content, a pair of nucleotides consisting of cytosine followed by guanine would be expected to occur 0.21 * 0.21 = 4.41% of the time. The frequency of CpG dinucleotides in human genomes is 1% — less than one-quarter of the expected frequency."[2]
Unmethylated CpG sites can be detected by Toll-Like Receptor 9[4] "(TLR 9) on plasmacytoid dendritic cells and B cells in humans. This is used to detect intracellular viral, fungal, and bacterial pathogen DNA."[2]
Methylation is central to imprinting, along with histone modifications.[5] Most of the methylation occurs a short distance from the CpG islands (at "CpG island shores") rather than in the islands themselves.[6]
Methylation of CpG sites within the promoters of genes can lead to their silencing, a feature found in a number of human cancers (for example the silencing of tumor suppressor genes). In contrast, the hypomethylation of CpG sites has been associated with the over-expression of oncogenes within cancer cells.[7]
"In eukaryotes, CpG methylation is an epigenetic DNA modification that is important for heterochromatin formation."[8]
"CENP-B preferentially binds to the unmethylated CENP-B box DNA."[8]
The "CpG methylations of the CENP-B box sequence may function in [RNA interference (RNAi)] RNAi-dependent heterochromatin formation by regulating CENP-B-binding to the CENP-B box sequence in the α-satellite repeats."[8]
Deamination
The CpG deficiency is due to an increased vulnerability of methylcytosines to spontaneously deaminate to thymine in genomes with CpG cytosine methylation.[9]
Ubiquitination
Phosphorylation
Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
See also
References
- ↑ Gerhard Leubner-Metzger, Luciana Petruzzelli, Rosa Waldvogel, Regina Vögeli-Lange, and Frederick Meins, Jr. (November 1998). "Ethylene-responsive element binding protein (EREBP) expression and the transcriptional regulation of class I β-1, 3-glucanase during tobacco seed germination". Plant Molecular Biology. 38 (5): 785–95. doi:10.1023/A:1006040425383. Retrieved 2014-05-02.
- ↑ 2.0 2.1 2.2 "CpG site". San Francisco, California: Wikimedia Foundation, Inc. January 30, 2013. Retrieved 2013-02-07.
- ↑ Jabbari K, Bernardi G (May 2004). "Cytosine methylation and CpG, TpG (CpA) and TpA frequencies". Gene. 333: 143–9. doi:10.1016/j.gene.2004.02.043. PMID 15177689.
- ↑ Ramirez-Ortiz ZG, Specht CA, Wang JP, Lee CK, Bartholomeu DC, Gazzinelli RT, Levitz SM (2008). "Toll-like receptor 9-dependent immune activation by unmethylated CpG motifs in Aspergillus fumigatus DNA". Infect Immun. 76 (5): 2123–9. doi:10.1128/IAI.00047-08. PMID 18332208.
- ↑ Feil R, Berger F (2007). "Convergent evolution of genomic imprinting in plants and mammals". Trends Genet. 23 (4): 192–9. doi:10.1016/j.tig.2007.02.004. PMID 17316885.
- ↑ Irizarry RA, Ladd-Acosta C, Wen B, Wu Z, Montano C, Onyango P, Cui H, Gabo K, Rongione M, Webster M, Ji H, Potash JB, Sabunciyan S, Feinberg AP (2009). "The human colon cancer methylome shows similar hypo- and hypermethylation at conserved tissue-specific CpG island shores". Nature Genetics. 41 (2): 178–86. PMID 19151715.
- ↑ Jones PA, Laird PW (February 1999). "Cancer epigenetics comes of age". Nat. Genet. 21 (2): 163–7. doi:10.1038/5947. PMID 9988266.
- ↑ 8.0 8.1 8.2 Yoshinori Tanaka, Hitoshi Kurumizaka, and Shigeyuki Yokoyama (2005). "CpG methylation of the CENP-B box reduces human CENP-B binding". The FEBS Journal. 272 (1): 282–289. doi:10.1111/j.1432-1033.2004.04406.x. PMID 15634350. Retrieved 2017-02-05. Unknown parameter
|month=ignored (help) - ↑ Scarano E, Iaccarino M, Grippo P, Parisi E (1967). "The heterogeneity of thymine methyl group origin in DNA pyrimidine isostichs of developing sea urchin embryos". Proceedings of the National Academy of Sciences USA. 57 (5): 1394–400. doi:10.1073/pnas.57.5.1394. PMC 224485. PMID 5231746.