SON (gene): Difference between revisions
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'''SON protein''' is a [[protein]] that in humans is encoded by the ''SON'' [[gene]].<ref name="pmid8318737">{{cite journal | author = Cheng S, Lutfalla G, Uze G, Chumakov IM, Gardiner K | title = GART, SON, IFNAR, and CRF2-4 genes cluster on human chromosome 21 and mouse chromosome 16 | journal = Mamm Genome | volume = 4 | issue = 6 | pages = 338–42 | year = 1993 | month = Aug | pmid = 8318737 | pmc = | doi =10.1007/BF00357094 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: SON SON DNA binding protein| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=6651| accessdate = }}</ref> |
'''SON protein''' is a [[protein]] that in humans is encoded by the ''SON'' [[gene]].<ref name="pmid8318737">{{cite journal | author = Cheng S, Lutfalla G, Uze G, Chumakov IM, Gardiner K | title = GART, SON, IFNAR, and CRF2-4 genes cluster on human chromosome 21 and mouse chromosome 16 | journal = Mamm Genome | volume = 4 | issue = 6 | pages = 338–42 | year = 1993 | month = Aug | pmid = 8318737 | pmc = | doi =10.1007/BF00357094 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: SON SON DNA binding protein| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=6651| accessdate = }}</ref> |
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SON is the name that has been given to a large Ser/Arg (SR)-related [[protein]], which is a [[RNA splicing|splicing]] co-factor that contributes to an efficient splicing within [[cell cycle]] progression.<ref name="Ahn_2011">{{cite journal | author = Ahn EY, DeKelver RC, Lo MC, Nguyen TA, Matsuura S, Boyapati A, Pandit S, Fu XD, Zhang DE | title = SON controls cell-cycle progression by coordinated regulation of RNA splicing | journal = Mol. Cell | volume = 42 | issue = 2 | pages = 185–98 | year = 2011 | month = April | pmid = 21504830 | pmc = 3137374 | doi = 10.1016/j.molcel.2011.03.014 }}</ref> It is also known as BASS1 (Bax antagonist selected in saccharomyces 1) or NRE-binding protein (Negative regulatory element-binding protein). The most common [[gene]] name of this splicing protein- which is only found in Humans (Homo sapiens)- is SON, but C21orf50, DBP5, KIAA1019 and NREBP can also be used as synonyms.<ref name="Son Human">{{cite web | url = http://www.uniprot.org/uniprot/P18583 | title = Protein SON | publisher = UniProt Consortium }}</ref> |
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== Presentation == |
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| ⚫ | The protein encoded by SON gene binds to a specific DNA sequence upstream of the upstream regulatory sequence of the core promoter and second enhancer of human [[hepatitis B virus]] (HBV). Through this binding, it represses HBV core promoter activity, transcription of HBV genes, and production of HBV virions. The protein shows sequence similarities with other DNA-binding structural proteins such as [[gallin]], [[oncoprotein]]s of the [[MYC]] family, and the oncoprotein [[MOS]]. It may also be involved in protecting cells from apoptosis and in pre-mRNA splicing.<ref name="entrez"/> |
||
SON is the name that has been given to a large Ser/Arg (SR)-related [[protein]], which is a [[RNA splicing|splicing]] co-factor that contributes to an efficient splicing within [[cell cycle]] progression.<ref name="ncbi.nlm.nih.gov">{{cite web|title=SON Controls Cell Cycle Progression by Coordinated Regulation of RNA Splicing|url=http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3137374/}}</ref> |
|||
It can also be called BASS1 (Bax antagonist selected in saccharomyces 1) or NRE-binding protein (Negative regulatory element-binding protein). The most common [[gene]] name of this splicing protein- which is only found in Humans (Homo sapiens)- is SON, but C21orf50, DBP5, KIAA1019 and NREBP can also be used as synonyms.<ref name="Son Human">{{cite web|title=Son Human|url=http://www.uniprot.org/uniprot/P18583}}</ref> |
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== Structure == |
== Structure == |
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The sequence length of the SON protein consists in 2426 [[aminoacids]] and its sequence status is totally completed. Its molecular weight is 263,830 Daltons (Da) and its domain contains 8 types of repeats which are distributed in 3 regions. This protein is found in the 21st [[chromosome]] and is mostly located in Nucleus speckle. Its higher expression is seen in leukocyte and heart.<ref name="Son Human"/><ref name="Son peptide">{{cite web|title=Son peptide|url=http://www.mybiosource.com/datasheet.php?products_id=427489}}</ref> |
The sequence length of the SON protein consists in 2426 [[aminoacids]] and its sequence status is totally completed. Its molecular weight is 263,830 Daltons (Da) and its domain contains 8 types of repeats which are distributed in 3 regions. This protein is found in the 21st [[chromosome]] and is mostly located in Nucleus speckle. Its higher expression is seen in leukocyte and heart.<ref name="Son Human"/><ref name="Son peptide">{{cite web | title = Son peptide | url = http://www.mybiosource.com/datasheet.php?products_id=427489 | publisher = MyBioSource.com }}</ref> |
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== Splicing process == |
== Splicing process == |
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Splicing is known as the process within the maturation of the pre-RNAm takes place. The pre-RNAm which has just been transcript has sequences called [[introns]] and [[exons]]. Introns are non-active nucleotide sequences that have to be removed in order the exons (active sequences) to get joined. This process must be very controlled. The splicing takes place in the [[spliceosome]], a complex that brings together a pre-RNAm and a variety of the binding proteins. These proteins together with the splicing factors (which are not found in the spliceosome) are in charge of recognizing the intron’s branch point sequence. The SON protein is known to be one of these binding proteins.<ref name="Donald V, Garden J. 2011"/> |
Splicing is known as the process within the maturation of the pre-RNAm takes place. The pre-RNAm which has just been transcript has sequences called [[introns]] and [[exons]]. Introns are non-active nucleotide sequences that have to be removed in order the exons (active sequences) to get joined. This process must be very controlled. The splicing takes place in the [[spliceosome]], a complex that brings together a pre-RNAm and a variety of the binding proteins. These proteins together with the splicing factors (which are not found in the spliceosome) are in charge of recognizing the intron’s branch point sequence. The SON protein is known to be one of these binding proteins.<ref name="Donald V, Garden J. 2011"/> |
||
Although there is a lack of knowledge about its exact splicing control in the progression of the cell cycle and it has remained largely unexplored, it’s certain that this splicing-associated protein is necessary for the maintenance of the embryonic stem cells because it influences the splicing of pluripotency regulators.<ref name=" |
Although there is a lack of knowledge about its exact splicing control in the progression of the cell cycle and it has remained largely unexplored, it’s certain that this splicing-associated protein is necessary for the maintenance of the embryonic stem cells because it influences the splicing of pluripotency regulators.<ref name="Ahn_2011"/><ref name="pmid24084863">{{cite journal | author = Livyatan I, Meshorer E | title = SON sheds light on RNA splicing and pluripotency | journal = Nat. Cell Biol. | volume = 15 | issue = 10 | pages = 1139–40 | year = 2013 | month = October | pmid = 24084863 | doi = 10.1038/ncb2851 }}</ref> |
||
SON plays an important role in the mRNA processing. Nevertheless, this process is still a little uncertain and this is why in a future it will be interesting to understand how exactly this protein interacts with the spliceosomal complex, its exact molecular function in the context of splicing. Not only the SON protein interferes in the splicing but also makes complex mechanisms such as the RNA post-transcriptional to cooperate with the splicing-mRNA processing.<ref name="Furukawa_2012">{{cite journal | author = Furukawa T, Tanji E, Kuboki Y, Hatori T, Yamamoto M, Shimizu K, Shibata N, Shiratori K | title = Targeting of MAPK-associated molecules identifies SON as a prime target to attenuate the proliferation and tumorigenicity of pancreatic cancer cells | journal = Mol. Cancer | volume = 11 | issue = | pages = 88 | year = 2012 | pmid = 23227827 | pmc = 3576306 | doi = 10.1186/1476-4598-11-88 }}</ref> |
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Human embryonic stem cells are able to undergo the process of differentiation into specific and relevant cells. To maintain the [[Pluripotency#Pluripotency |pluripotency]] of the embryonic stem cells, transcription factors and epigenetic modifiers play an important role despite the fact that little is known about the regulation of pluripotency throughout the process of splicing. The factor SON is identified as essential for the maintenance of this pluripotency. It is confirmed that SON regulates the splicing process of transcripts (RNAm) that will encode the gens that are going to regulate the pluripotency of the embryonic human cells.<ref>{{cite |
Human embryonic stem cells are able to undergo the process of differentiation into specific and relevant cells. To maintain the [[Pluripotency#Pluripotency |pluripotency]] of the embryonic stem cells, transcription factors and epigenetic modifiers play an important role despite the fact that little is known about the regulation of pluripotency throughout the process of splicing. The factor SON is identified as essential for the maintenance of this pluripotency. It is confirmed that SON regulates the splicing process of transcripts (RNAm) that will encode the gens that are going to regulate the pluripotency of the embryonic human cells.<ref name="pmid24013217">{{cite journal | author = Lu X, Göke J, Sachs F, Jacques PÉ, Liang H, Feng B, Bourque G, Bubulya PA, Ng HH | title = SON connects the splicing-regulatory network with pluripotency in human embryonic stem cells | journal = Nat. Cell Biol. | volume = 15 | issue = 10 | pages = 1141–52 | year = 2013 | month = October | pmid = 24013217 | doi = 10.1038/ncb2839 }}</ref> |
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== |
== Function == |
||
[[File:SONprotein3.png|200px|right|thumb|SON protein's intervention in the splicing process.]] |
[[File:SONprotein3.png|200px|right|thumb|SON protein's intervention in the splicing process.]] |
||
On the one hand, SON protein is required to maintain the genome stability in order to ensure an efficient RNA processing of affected genes. It also facilitates the interaction of SR proteins with [[RNA polymerase II]] and is required for processing of weak constitutive splice sites, having also strong implications in cancer and other human diseases.<ref name=" |
On the one hand, SON protein is required to maintain the genome stability in order to ensure an efficient RNA processing of affected genes. It also facilitates the interaction of SR proteins with [[RNA polymerase II]] and is required for processing of weak constitutive splice sites, having also strong implications in cancer and other human diseases.<ref name="Ahn_2011"/><ref name="Son peptide"/> |
||
On the other side, a deficiency or knockdown of SON protein causes various and severe defects in mitotic division arrangement, chromosome alignment and microtubule dynamics when spindle pole separation takes place.<ref name=" |
On the other side, a deficiency or knockdown of SON protein causes various and severe defects in mitotic division arrangement, chromosome alignment and microtubule dynamics when spindle pole separation takes place.<ref name="Ahn_2011"/> |
||
But as we could read in the article called “SON protein regulates GATA-2 through transcriptional control of the microRNA 23a-27-24-a clúster”, SON protein has even more functions in the organism. It has been found that these proteins may regulate the hematopoietic cells [https://en.wikipedia.org/wiki/Cell_differentiation differentiation]. They have a specific job in [[Hematopoiesis|hematopoietic process]], which is based on activating other proteins called GATA. As these ones are finally activated, the cell differentiation starts normally.<ref>{{cite |
But as we could read in the article called “SON protein regulates GATA-2 through transcriptional control of the microRNA 23a-27-24-a clúster”, SON protein has even more functions in the organism. It has been found that these proteins may regulate the hematopoietic cells [https://en.wikipedia.org/wiki/Cell_differentiation differentiation]. They have a specific job in [[Hematopoiesis|hematopoietic process]], which is based on activating other proteins called GATA. As these ones are finally activated, the cell differentiation starts normally.<ref name="pmid23322776">{{cite journal | author = Ahn EE, Higashi T, Yan M, Matsuura S, Hickey CJ, Lo MC, Shia WJ, DeKelver RC, Zhang DE | title = SON protein regulates GATA-2 through transcriptional control of the microRNA 23a~27a~24-2 cluster | journal = J. Biol. Chem. | volume = 288 | issue = 8 | pages = 5381–8 | year = 2013 | month = February | pmid = 23322776 | doi = 10.1074/jbc.M112.447227 }}</ref> |
||
== |
== Clinical significance == |
||
A recent study suggested that SON may be a novel therapeutic molecular target for pancreatic cancer as the results of a recent study show that this protein is very important as far as proliferation, survival and tumorigenicity of cancer cells are concerned. Specifically, these results revealed that the serine-arginine-rich protein involved in the RNA splicing process, could suppress pancreatic cell tumorigenicity.<ref name=" |
A recent study suggested that SON may be a novel therapeutic molecular target for pancreatic cancer as the results of a recent study show that this protein is very important as far as proliferation, survival and tumorigenicity of cancer cells are concerned. Specifically, these results revealed that the serine-arginine-rich protein involved in the RNA splicing process, could suppress pancreatic cell tumorigenicity.<ref name="Furukawa_2012"/> |
||
| ⚫ | The protein encoded by SON gene binds to a specific DNA sequence upstream of the upstream regulatory sequence of the core promoter and second enhancer of human hepatitis B virus (HBV). Through this binding, it represses HBV core promoter activity, transcription of HBV genes, and production of HBV virions. The protein shows sequence similarities with other DNA-binding structural proteins such as gallin, |
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== References == |
== References == |
||
| ⚫ | |||
| ⚫ | |||
== Further reading == |
== Further reading == |
||
{{refbegin |
{{refbegin|35em}} |
||
*{{cite journal | author=Mattioni T, Hume CR, Konigorski S, ''et al.'' |title=A cDNA clone for a novel nuclear protein with DNA binding activity. |journal=Chromosoma |volume=101 |issue= 10 |pages= 618–24 |year= 1992 |pmid= 1424986 |doi=10.1007/BF00360539 }} |
*{{cite journal | author=Mattioni T, Hume CR, Konigorski S, ''et al.'' |title=A cDNA clone for a novel nuclear protein with DNA binding activity. |journal=Chromosoma |volume=101 |issue= 10 |pages= 618–24 |year= 1992 |pmid= 1424986 |doi=10.1007/BF00360539 }} |
||
*{{cite journal | author=Bliskovskiĭ VV, Berdichevskiĭ FB, Tkachenko AV, ''et al.'' |title=[Coding part of the son gene small transcript contains four areas of complete tandem repeats] |journal=Mol. Biol. (Mosk.) |volume=26 |issue= 4 |pages= 793–806 |year= 1992 |pmid= 1435773 |doi= }} |
*{{cite journal | author=Bliskovskiĭ VV, Berdichevskiĭ FB, Tkachenko AV, ''et al.'' |title=[Coding part of the son gene small transcript contains four areas of complete tandem repeats] |journal=Mol. Biol. (Mosk.) |volume=26 |issue= 4 |pages= 793–806 |year= 1992 |pmid= 1435773 |doi= }} |
||
Revision as of 05:44, 25 October 2013
Template:PBB SON protein is a protein that in humans is encoded by the SON gene.[1][2]
SON is the name that has been given to a large Ser/Arg (SR)-related protein, which is a splicing co-factor that contributes to an efficient splicing within cell cycle progression.[3] It is also known as BASS1 (Bax antagonist selected in saccharomyces 1) or NRE-binding protein (Negative regulatory element-binding protein). The most common gene name of this splicing protein- which is only found in Humans (Homo sapiens)- is SON, but C21orf50, DBP5, KIAA1019 and NREBP can also be used as synonyms.[4]
The protein encoded by SON gene binds to a specific DNA sequence upstream of the upstream regulatory sequence of the core promoter and second enhancer of human hepatitis B virus (HBV). Through this binding, it represses HBV core promoter activity, transcription of HBV genes, and production of HBV virions. The protein shows sequence similarities with other DNA-binding structural proteins such as gallin, oncoproteins of the MYC family, and the oncoprotein MOS. It may also be involved in protecting cells from apoptosis and in pre-mRNA splicing.[2]
Structure
The sequence length of the SON protein consists in 2426 aminoacids and its sequence status is totally completed. Its molecular weight is 263,830 Daltons (Da) and its domain contains 8 types of repeats which are distributed in 3 regions. This protein is found in the 21st chromosome and is mostly located in Nucleus speckle. Its higher expression is seen in leukocyte and heart.[4][5]
Splicing process
SON protein is essential for maintaining the subnuclear organization of the factors that are processed in the nucleus highlighting its direct role in pre-mRNA splicing.[6]
Splicing is known as the process within the maturation of the pre-RNAm takes place. The pre-RNAm which has just been transcript has sequences called introns and exons. Introns are non-active nucleotide sequences that have to be removed in order the exons (active sequences) to get joined. This process must be very controlled. The splicing takes place in the spliceosome, a complex that brings together a pre-RNAm and a variety of the binding proteins. These proteins together with the splicing factors (which are not found in the spliceosome) are in charge of recognizing the intron’s branch point sequence. The SON protein is known to be one of these binding proteins.[6]
Although there is a lack of knowledge about its exact splicing control in the progression of the cell cycle and it has remained largely unexplored, it’s certain that this splicing-associated protein is necessary for the maintenance of the embryonic stem cells because it influences the splicing of pluripotency regulators.[3][7]
SON plays an important role in the mRNA processing. Nevertheless, this process is still a little uncertain and this is why in a future it will be interesting to understand how exactly this protein interacts with the spliceosomal complex, its exact molecular function in the context of splicing. Not only the SON protein interferes in the splicing but also makes complex mechanisms such as the RNA post-transcriptional to cooperate with the splicing-mRNA processing.[8]
Human embryonic stem cells are able to undergo the process of differentiation into specific and relevant cells. To maintain the pluripotency of the embryonic stem cells, transcription factors and epigenetic modifiers play an important role despite the fact that little is known about the regulation of pluripotency throughout the process of splicing. The factor SON is identified as essential for the maintenance of this pluripotency. It is confirmed that SON regulates the splicing process of transcripts (RNAm) that will encode the gens that are going to regulate the pluripotency of the embryonic human cells.[9]
Function
On the one hand, SON protein is required to maintain the genome stability in order to ensure an efficient RNA processing of affected genes. It also facilitates the interaction of SR proteins with RNA polymerase II and is required for processing of weak constitutive splice sites, having also strong implications in cancer and other human diseases.[3][5]
On the other side, a deficiency or knockdown of SON protein causes various and severe defects in mitotic division arrangement, chromosome alignment and microtubule dynamics when spindle pole separation takes place.[3]
But as we could read in the article called “SON protein regulates GATA-2 through transcriptional control of the microRNA 23a-27-24-a clúster”, SON protein has even more functions in the organism. It has been found that these proteins may regulate the hematopoietic cells differentiation. They have a specific job in hematopoietic process, which is based on activating other proteins called GATA. As these ones are finally activated, the cell differentiation starts normally.[10]
Clinical significance
A recent study suggested that SON may be a novel therapeutic molecular target for pancreatic cancer as the results of a recent study show that this protein is very important as far as proliferation, survival and tumorigenicity of cancer cells are concerned. Specifically, these results revealed that the serine-arginine-rich protein involved in the RNA splicing process, could suppress pancreatic cell tumorigenicity.[8]
References
- ^ Cheng S, Lutfalla G, Uze G, Chumakov IM, Gardiner K (1993). "GART, SON, IFNAR, and CRF2-4 genes cluster on human chromosome 21 and mouse chromosome 16". Mamm Genome. 4 (6): 338–42. doi:10.1007/BF00357094. PMID 8318737.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b "Entrez Gene: SON SON DNA binding protein".
- ^ a b c d Ahn EY, DeKelver RC, Lo MC, Nguyen TA, Matsuura S, Boyapati A, Pandit S, Fu XD, Zhang DE (2011). "SON controls cell-cycle progression by coordinated regulation of RNA splicing". Mol. Cell. 42 (2): 185–98. doi:10.1016/j.molcel.2011.03.014. PMC 3137374. PMID 21504830.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ a b "Protein SON". UniProt Consortium.
- ^ a b "Son peptide". MyBioSource.com.
- ^ a b Donald V, Garden J. (2011). Biochemistry. USA: John Wiley & Sons. ISBN 9780470-57095-1.
- ^ Livyatan I, Meshorer E (2013). "SON sheds light on RNA splicing and pluripotency". Nat. Cell Biol. 15 (10): 1139–40. doi:10.1038/ncb2851. PMID 24084863.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ a b Furukawa T, Tanji E, Kuboki Y, Hatori T, Yamamoto M, Shimizu K, Shibata N, Shiratori K (2012). "Targeting of MAPK-associated molecules identifies SON as a prime target to attenuate the proliferation and tumorigenicity of pancreatic cancer cells". Mol. Cancer. 11: 88. doi:10.1186/1476-4598-11-88. PMC 3576306. PMID 23227827.
{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - ^ Lu X, Göke J, Sachs F, Jacques PÉ, Liang H, Feng B, Bourque G, Bubulya PA, Ng HH (2013). "SON connects the splicing-regulatory network with pluripotency in human embryonic stem cells". Nat. Cell Biol. 15 (10): 1141–52. doi:10.1038/ncb2839. PMID 24013217.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Ahn EE, Higashi T, Yan M, Matsuura S, Hickey CJ, Lo MC, Shia WJ, DeKelver RC, Zhang DE (2013). "SON protein regulates GATA-2 through transcriptional control of the microRNA 23a~27a~24-2 cluster". J. Biol. Chem. 288 (8): 5381–8. doi:10.1074/jbc.M112.447227. PMID 23322776.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
Further reading
- Mattioni T, Hume CR, Konigorski S; et al. (1992). "A cDNA clone for a novel nuclear protein with DNA binding activity". Chromosoma. 101 (10): 618–24. doi:10.1007/BF00360539. PMID 1424986.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Bliskovskiĭ VV, Berdichevskiĭ FB, Tkachenko AV; et al. (1992). "[Coding part of the son gene small transcript contains four areas of complete tandem repeats]". Mol. Biol. (Mosk.). 26 (4): 793–806. PMID 1435773.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Bliskovskiĭ VV, Kirillov AV, Zakhar'ev VM, Chumankov IM (1992). "[The human son gene: the large and small transcripts contains various 5'-terminal sequences]". Mol. Biol. (Mosk.). 26 (4): 807–12. PMID 1435774.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - Tassone F, Cheng S, Gardiner K (1993). "Analysis of chromosome 21 yeast artificial chromosome (YAC) clones". Am. J. Hum. Genet. 51 (6): 1251–64. PMC 1682922. PMID 1463009.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - Chumakov IM, Berdichevskiĭ FB, Sokolova NV; et al. (1991). "[Identification of a protein product of a novel human gene SON and the biological effect upon administering a changed form of this gene into mammalian cells]". Mol. Biol. (Mosk.). 25 (3): 731–9. PMID 1944255.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Berdichevskiĭ FB, Chumakov IM, Kiselev LL (1988). "[Decoding of the primary structure of the son3 region in human genome: identification of a new protein with unusual structure and homology with DNA-binding proteins]". Mol. Biol. (Mosk.). 22 (3): 794–801. PMID 3054499.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - Khan IM, Fisher RA, Johnson KJ; et al. (1994). "The SON gene encodes a conserved DNA binding protein mapping to human chromosome 21". Ann. Hum. Genet. 58 (Pt 1): 25–34. doi:10.1111/j.1469-1809.1994.tb00723.x. PMID 8031013.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Kikuno R, Nagase T, Ishikawa K; et al. (1999). "Prediction of the coding sequences of unidentified human genes. XIV. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Res. 6 (3): 197–205. doi:10.1093/dnares/6.3.197. PMID 10470851.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Greenhalf W, Lee J, Chaudhuri B (1999). "A selection system for human apoptosis inhibitors using yeast". Yeast. 15 (13): 1307–21. doi:10.1002/(SICI)1097-0061(19990930)15:13<1307::AID-YEA455>3.0.CO;2-3. PMID 10509013.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - Hattori M, Fujiyama A, Taylor TD; et al. (2000). "The DNA sequence of human chromosome 21". Nature. 405 (6784): 311–9. doi:10.1038/35012518. PMID 10830953.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Wynn SL, Fisher RA, Pagel C; et al. (2001). "Organization and conservation of the GART/SON/DONSON locus in mouse and human genomes". Genomics. 68 (1): 57–62. doi:10.1006/geno.2000.6254. PMID 10950926.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Sun CT, Lo WY, Wang IH; et al. (2001). "Transcription repression of human hepatitis B virus genes by negative regulatory element-binding protein/SON". J. Biol. Chem. 276 (26): 24059–67. doi:10.1074/jbc.M101330200. PMID 11306577.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - Reymond A, Friedli M, Henrichsen CN; et al. (2002). "From PREDs and open reading frames to cDNA isolation: revisiting the human chromosome 21 transcription map". Genomics. 78 (1–2): 46–54. doi:10.1006/geno.2001.6640. PMID 11707072.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Yi J, Kloeker S, Jensen CC; et al. (2002). "Members of the Zyxin family of LIM proteins interact with members of the p130Cas family of signal transducers". J. Biol. Chem. 277 (11): 9580–9. doi:10.1074/jbc.M106922200. PMID 11782456.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - Strausberg RL, Feingold EA, Grouse LH; et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Casadei R, Strippoli P, D'Addabbo P; et al. (2004). "mRNA 5' region sequence incompleteness: a potential source of systematic errors in translation initiation codon assignment in human mRNAs". Gene. 321: 185–93. doi:10.1016/S0378-1119(03)00835-7. PMID 14637006.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Ota T, Suzuki Y, Nishikawa T; et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs". Nat. Genet. 36 (1): 40–5. doi:10.1038/ng1285. PMID 14702039.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link) - Hillman RT, Green RE, Brenner SE (2005). "An unappreciated role for RNA surveillance". Genome Biol. 5 (2): R8. doi:10.1186/gb-2004-5-2-r8. PMC 395752. PMID 14759258.
{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link) - Colland F, Jacq X, Trouplin V; et al. (2004). "Functional proteomics mapping of a human signaling pathway". Genome Res. 14 (7): 1324–32. doi:10.1101/gr.2334104. PMC 442148. PMID 15231748.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: multiple names: authors list (link)
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