ARL4D: Difference between revisions

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{{Infobox_gene}}
{{PBB_Controls
'''ADP-ribosylation factor-like protein 4D''' is a [[protein]] that in humans is encoded by the ''ARL4D'' [[gene]].<ref name="pmid7590735">{{cite journal | vauthors = Smith SA, Holik PR, Stevens J, Melis R, White R, Albertsen H | title = Isolation and mapping of a gene encoding a novel human ADP-ribosylation factor on chromosome 17q12-q21 | journal = Genomics | volume = 28 | issue = 1 | pages = 113–5 | date = Jul 1995 | pmid = 7590735 | pmc =  | doi = 10.1006/geno.1995.1115 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: ARL4D ADP-ribosylation factor-like 4D| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=379| accessdate = }}</ref>
| update_page = yes
| require_manual_inspection = no
| update_protein_box = yes
| update_summary = yes
| update_citations = yes
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<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
== Function ==
{{GNF_Protein_box
| image =
| image_source =
| PDB =
| Name = ADP-ribosylation factor-like 4D
| HGNCid = 656
| Symbol = ARL4D
| AltSymbols =; ARF4L; ARL6
| OMIM = 600732
| ECnumber = 
| Homologene = 1255
| MGIid = 1933155
| GeneAtlas_image1 = PBB_GE_ARL4D_203586_s_at_tn.png
| Function = {{GNF_GO|id=GO:0000166 |text = nucleotide binding}} {{GNF_GO|id=GO:0003924 |text = GTPase activity}} {{GNF_GO|id=GO:0005525 |text = GTP binding}}
| Component = {{GNF_GO|id=GO:0005622 |text = intracellular}} {{GNF_GO|id=GO:0005634 |text = nucleus}}
| Process = {{GNF_GO|id=GO:0007264 |text = small GTPase mediated signal transduction}} {{GNF_GO|id=GO:0009306 |text = protein secretion}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 379
    | Hs_Ensembl = ENSG00000175906
    | Hs_RefseqProtein = NP_001652
    | Hs_RefseqmRNA = NM_001661
    | Hs_GenLoc_db = 
    | Hs_GenLoc_chr = 17
    | Hs_GenLoc_start = 38831879
    | Hs_GenLoc_end = 38834029
    | Hs_Uniprot = P49703
    | Mm_EntrezGene = 80981
    | Mm_Ensembl = 
    | Mm_RefseqmRNA = NM_031160
    | Mm_RefseqProtein = NP_112437
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 
    | Mm_GenLoc_start = 
    | Mm_GenLoc_end = 
    | Mm_Uniprot = 
  }}
}}
'''ADP-ribosylation factor-like 4D''', also known as '''ARL4D''', is a human [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: ARL4D ADP-ribosylation factor-like 4D| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=379| accessdate = }}</ref>


<!-- The PBB_Summary template is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
ADP-ribosylation factor 4D is a member of the ADP-ribosylation factor family of GTP-binding proteins. ARL4D is closely similar to [[ARL4A]] and ARL4C and each has a nuclear localization signal and an unusually high guanine nucleotide exchange rate. This protein may play a role in membrane-associated intracellular trafficking. Mutations in this gene have been associated with [[Bardet–Biedl syndrome]] (BBS).<ref name="entrez"/>
{{PBB_Summary
==Model organisms==
| section_title =
{| class="wikitable sortable collapsible collapsed" border="1" cellpadding="2" style="float: right;" |
| summary_text = ADP-ribosylation factor 4D is a member of the ADP-ribosylation factor family of GTP-binding proteins. ARL4D is closely similar to ARL4A and ARL4C and each has a nuclear localization signal and an unusually high guanine nucleotide exchange rate. This protein may play a role in membrane-associated intracellular trafficking. Mutations in this gene have been associated with Bardet-Biedl syndrome (BBS).<ref name="entrez">{{cite web | title = Entrez Gene: ARL4D ADP-ribosylation factor-like 4D| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=379| accessdate = }}</ref>
|+ ''Arl4d'' knockout mouse phenotype
}}
|-
! Characteristic!! Phenotype


==References==
|-
{{reflist|2}}
| [[Homozygote]] viability || bgcolor="#488ED3"|Normal
==Further reading==
|-
| Fertility || bgcolor="#488ED3"|Normal
|-
| Body weight || bgcolor="#488ED3"|Normal
|-
| [[Open_Field_(animal_test)|Anxiety]] || bgcolor="#488ED3"|Normal
|-
| Neurological assessment || bgcolor="#488ED3"|Normal
|-
| Grip strength || bgcolor="#488ED3"|Normal
|-
| [[Hot_plate_test|Hot plate]] || bgcolor="#488ED3"|Normal
|-
| [[Dysmorphology]] || bgcolor="#488ED3"|Normal
|-
| [[Indirect calorimetry]] || bgcolor="#488ED3"|Normal
|-
| [[Glucose tolerance test]] || bgcolor="#488ED3"|Normal
|-
| [[Auditory brainstem response]] || bgcolor="#488ED3"|Normal
|-
| [[Dual-energy_X-ray_absorptiometry|DEXA]] || bgcolor="#C40000"|Abnormal<ref name="DEXA">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBTW/body-composition-dexa/ |title=DEXA data for Arl4d |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| [[Radiography]] || bgcolor="#C40000"|Abnormal<ref name="Radiography">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBTW/x-ray-imaging/ |title=Radiography data for Arl4d |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| Body temperature || bgcolor="#488ED3"|Normal
|-
| Eye morphology || bgcolor="#488ED3"|Normal
|-
| [[Clinical chemistry]] || bgcolor="#488ED3"|Normal
|-
| [[Haematology]] || bgcolor="#488ED3"|Normal
|-
| [[Peripheral blood lymphocyte]]s || bgcolor="#C40000"|Abnormal<ref name="Peripheral blood lymphocytes">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBTW/peripheral-blood-lymphocytes/ |title=Peripheral blood lymphocytes data for Arl4d |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| [[Micronucleus test]] || bgcolor="#488ED3"|Normal
|-
| Heart weight || bgcolor="#C40000"|Abnormal<ref name="Heart weight">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBTW/heart-weight/ |title=Heart weight data for Arl4d |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| Skin Histopathology || bgcolor="#488ED3"|Normal
|-
| Brain histopathology || bgcolor="#C40000"|Abnormal
|-
| Eye Histopathology || bgcolor="#488ED3"|Normal
|-
| ''[[Salmonella]]'' infection || bgcolor="#488ED3"|Normal<ref name="''Salmonella'' infection">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBTW/salmonella-challenge/ |title=''Salmonella'' infection data for Arl4d |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| ''[[Citrobacter]]'' infection || bgcolor="#488ED3"|Normal<ref name="''Citrobacter'' infection">{{cite web |url=http://www.sanger.ac.uk/mouseportal/phenotyping/MBTW/citrobacter-challenge/ |title=''Citrobacter'' infection data for Arl4d |publisher=Wellcome Trust Sanger Institute}}</ref>
|-
| colspan=2; style="text-align: center;" | All tests and analysis from<ref name="mgp_reference">{{cite journal | doi = 10.1111/j.1755-3768.2010.4142.x | title = The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice | year = 2010 | author = Gerdin AK | journal = Acta Ophthalmologica | volume = 88 | pages =  925–7 }}</ref><ref>[http://www.sanger.ac.uk/mouseportal/ Mouse Resources Portal], Wellcome Trust Sanger Institute.</ref>
|}
[[Model organism]]s have been used in the study of ARL4D function. A conditional [[knockout mouse]] line, called ''Arl4d<sup>tm1a(EUCOMM)Wtsi</sup>''<ref name="allele_ref">{{cite web |url=http://www.knockoutmouse.org/martsearch/search?query=Arl4d |title=International Knockout Mouse Consortium}}</ref><ref name="mgi_allele_ref">{{cite web |url=http://www.informatics.jax.org/searchtool/Search.do?query=MGI:4432430 |title=Mouse Genome Informatics}}</ref> was generated as part of the [[International Knockout Mouse Consortium]] program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.<ref name="pmid21677750">{{cite journal | vauthors = Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A | title = A conditional knockout resource for the genome-wide study of mouse gene function | journal = Nature | volume = 474 | issue = 7351 | pages = 337–42 | date = Jun 2011 | pmid = 21677750 | pmc = 3572410 | doi = 10.1038/nature10163 }}</ref><ref name="mouse_library">{{cite journal | vauthors = Dolgin E | title = Mouse library set to be knockout | journal = Nature | volume = 474 | issue = 7351 | pages = 262–3 | date = Jun 2011 | pmid = 21677718 | doi = 10.1038/474262a }}</ref><ref name="mouse_for_all_reasons">{{cite journal | vauthors = Collins FS, Rossant J, Wurst W | title = A mouse for all reasons | journal = Cell | volume = 128 | issue = 1 | pages = 9–13 | date = Jan 2007 | pmid = 17218247 | doi = 10.1016/j.cell.2006.12.018 }}</ref>
 
Male and female animals underwent a standardized [[phenotypic screen]] to determine the effects of deletion.<ref name="mgp_reference" /><ref name="pmid21722353">{{cite journal | vauthors = van der Weyden L, White JK, Adams DJ, Logan DW | title = The mouse genetics toolkit: revealing function and mechanism | journal = Genome Biology | volume = 12 | issue = 6 | pages = 224 | year = 2011 | pmid = 21722353 | pmc = 3218837 | doi = 10.1186/gb-2011-12-6-224 }} </ref> Twenty five tests were carried out on [[mutant]] mice and significant abnormalities were observed.<ref name="mgp_reference" /> [[Homozygous]] mutant females had decreased bone mineral content, heart weight, lean body mass and CD8-positive, alpha-beta memory [[T cell]] number. Males had abnormal rib morphology with vertebral transformation. Both sexes displayed a reduction in dorsal [[third ventricle]] area and [[hippocampal]] area.<ref name="mgp_reference" />
 
== References ==
{{reflist}}
 
==External links==
* {{UCSC gene info|ARL4D}}
* {{UCSC gene info|ARL6}}
 
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
{{PBB_Further_reading
* {{cite journal | vauthors = Miki Y, Swensen J, Shattuck-Eidens D, Futreal PA, Harshman K, Tavtigian S, Liu Q, Cochran C, Bennett LM, Ding W | title = A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1 | journal = Science | volume = 266 | issue = 5182 | pages = 66–71 | date = Oct 1994 | pmid = 7545954 | doi = 10.1126/science.7545954 }}
| citations =
* {{cite journal | vauthors = Harshman K, Bell R, Rosenthal J, Katcher H, Miki Y, Swenson J, Gholami Z, Frye C, Ding W, Dayananth P | title = Comparison of the positional cloning methods used to isolate the BRCA1 gene | journal = Human Molecular Genetics | volume = 4 | issue = 8 | pages = 1259–66 | date = Aug 1995 | pmid = 7581362 | doi = 10.1093/hmg/4.8.1259 }}
*{{cite journal | author=Miki Y, Swensen J, Shattuck-Eidens D, ''et al.'' |title=A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. |journal=Science |volume=266 |issue= 5182 |pages= 66-71 |year= 1994 |pmid= 7545954 |doi= }}
* {{cite journal | vauthors = Bonaldo MF, Lennon G, Soares MB | title = Normalization and subtraction: two approaches to facilitate gene discovery | journal = Genome Research | volume = 6 | issue = 9 | pages = 791–806 | date = Sep 1996 | pmid = 8889548 | doi = 10.1101/gr.6.9.791 }}
*{{cite journal | author=Harshman K, Bell R, Rosenthal J, ''et al.'' |title=Comparison of the positional cloning methods used to isolate the BRCA1 gene. |journal=Hum. Mol. Genet. |volume=4 |issue= 8 |pages= 1259-66 |year= 1995 |pmid= 7581362 |doi=  }}
* {{cite journal | vauthors = Jacobs S, Schilf C, Fliegert F, Koling S, Weber Y, Schürmann A, Joost HG | title = ADP-ribosylation factor (ARF)-like 4, 6, and 7 represent a subgroup of the ARF family characterization by rapid nucleotide exchange and a nuclear localization signal | journal = FEBS Letters | volume = 456 | issue = 3 | pages = 384–8 | date = Aug 1999 | pmid = 10462049 | doi = 10.1016/S0014-5793(99)00759-0 }}
*{{cite journal  | author=Smith SA, Holik PR, Stevens J, ''et al.'' |title=Isolation and mapping of a gene encoding a novel human ADP-ribosylation factor on chromosome 17q12-q21. |journal=Genomics |volume=28 |issue= 1 |pages= 113-5 |year= 1995 |pmid= 7590735 |doi= 10.1006/geno.1995.1115 }}
* {{cite journal | vauthors = Ingley E, Williams JH, Walker CE, Tsai S, Colley S, Sayer MS, Tilbrook PA, Sarna M, Beaumont JG, Klinken SP | title = A novel ADP-ribosylation like factor (ARL-6), interacts with the protein-conducting channel SEC61beta subunit | journal = FEBS Letters | volume = 459 | issue = 1 | pages = 69–74 | date = Oct 1999 | pmid = 10508919 | doi = 10.1016/S0014-5793(99)01188-6 }}
*{{cite journal | author=Bonaldo MF, Lennon G, Soares MB |title=Normalization and subtraction: two approaches to facilitate gene discovery. |journal=Genome Res. |volume=6 |issue= 9 |pages= 791-806 |year= 1997 |pmid= 8889548 |doi= }}
* {{cite journal | vauthors = Nonaka Y, Tsuda N, Shichijo S, Ito M, Maeda Y, Harada M, Kamura T, Shigemori M, Itoh K | title = Recognition of ADP-ribosylation factor 4-like by HLA-A2-restricted and tumor-reactive cytotoxic T lymphocytes from patients with brain tumors | journal = Tissue Antigens | volume = 60 | issue = 4 | pages = 319–27 | date = Oct 2002 | pmid = 12472661 | doi = 10.1034/j.1399-0039.2002.600406.x }}
*{{cite journal | author=Jacobs S, Schilf C, Fliegert F, ''et al.'' |title=ADP-ribosylation factor (ARF)-like 4, 6, and 7 represent a subgroup of the ARF family characterization by rapid nucleotide exchange and a nuclear localization signal. |journal=FEBS Lett. |volume=456 |issue= 3 |pages= 384-8 |year= 1999 |pmid= 10462049 |doi= }}
* {{cite journal | vauthors = Chiang AP, Nishimura D, Searby C, Elbedour K, Carmi R, Ferguson AL, Secrist J, Braun T, Casavant T, Stone EM, Sheffield VC | title = Comparative genomic analysis identifies an ADP-ribosylation factor-like gene as the cause of Bardet-Biedl syndrome (BBS3) | journal = American Journal of Human Genetics | volume = 75 | issue = 3 | pages = 475–84 | date = Sep 2004 | pmid = 15258860 | pmc = 1182025 | doi = 10.1086/423903 }}
*{{cite journal | author=Ingley E, Williams JH, Walker CE, ''et al.'' |title=A novel ADP-ribosylation like factor (ARL-6), interacts with the protein-conducting channel SEC61beta subunit. |journal=FEBS Lett. |volume=459 |issue= 1 |pages= 69-74 |year= 1999 |pmid= 10508919 |doi= }}
* {{cite journal | vauthors = Fan Y, Esmail MA, Ansley SJ, Blacque OE, Boroevich K, Ross AJ, Moore SJ, Badano JL, May-Simera H, Compton DS, Green JS, Lewis RA, van Haelst MM, Parfrey PS, Baillie DL, Beales PL, Katsanis N, Davidson WS, Leroux MR | title = Mutations in a member of the Ras superfamily of small GTP-binding proteins causes Bardet-Biedl syndrome | journal = Nature Genetics | volume = 36 | issue = 9 | pages = 989–93 | date = Sep 2004 | pmid = 15314642 | doi = 10.1038/ng1414 }}
*{{cite journal | author=Nonaka Y, Tsuda N, Shichijo S, ''et al.'' |title=Recognition of ADP-ribosylation factor 4-like by HLA-A2-restricted and tumor-reactive cytotoxic T lymphocytes from patients with brain tumors. |journal=Tissue Antigens |volume=60 |issue= 4 |pages= 319-27 |year= 2003 |pmid= 12472661 |doi= }}
* {{cite journal | vauthors = Rual JF, Venkatesan K, Hao T, Hirozane-Kishikawa T, Dricot A, Li N, Berriz GF, Gibbons FD, Dreze M, Ayivi-Guedehoussou N, Klitgord N, Simon C, Boxem M, Milstein S, Rosenberg J, Goldberg DS, Zhang LV, Wong SL, Franklin G, Li S, Albala JS, Lim J, Fraughton C, Llamosas E, Cevik S, Bex C, Lamesch P, Sikorski RS, Vandenhaute J, Zoghbi HY, Smolyar A, Bosak S, Sequerra R, Doucette-Stamm L, Cusick ME, Hill DE, Roth FP, Vidal M | title = Towards a proteome-scale map of the human protein-protein interaction network | journal = Nature | volume = 437 | issue = 7062 | pages = 1173–8 | date = Oct 2005 | pmid = 16189514 | doi = 10.1038/nature04209 }}
*{{cite journal  | author=Strausberg RL, Feingold EA, Grouse LH, ''et al.'' |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899-903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899 }}
* {{cite journal | vauthors = Hofmann I, Thompson A, Sanderson CM, Munro S | title = The Arl4 family of small G proteins can recruit the cytohesin Arf6 exchange factors to the plasma membrane | journal = Current Biology | volume = 17 | issue = 8 | pages = 711–6 | date = Apr 2007 | pmid = 17398095 | doi = 10.1016/j.cub.2007.03.007 }}
*{{cite journal | author=Chiang AP, Nishimura D, Searby C, ''et al.'' |title=Comparative genomic analysis identifies an ADP-ribosylation factor-like gene as the cause of Bardet-Biedl syndrome (BBS3). |journal=Am. J. Hum. Genet. |volume=75 |issue= 3 |pages= 475-84 |year= 2004 |pmid= 15258860 |doi= 10.1086/423903 }}
*{{cite journal | author=Fan Y, Esmail MA, Ansley SJ, ''et al.'' |title=Mutations in a member of the Ras superfamily of small GTP-binding proteins causes Bardet-Biedl syndrome. |journal=Nat. Genet. |volume=36 |issue= 9 |pages= 989-93 |year= 2004 |pmid= 15314642 |doi= 10.1038/ng1414 }}
*{{cite journal | author=Gerhard DS, Wagner L, Feingold EA, ''et al.'' |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121-7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 }}
*{{cite journal  | author=Rual JF, Venkatesan K, Hao T, ''et al.'' |title=Towards a proteome-scale map of the human protein-protein interaction network. |journal=Nature |volume=437 |issue= 7062 |pages= 1173-8 |year= 2005 |pmid= 16189514 |doi= 10.1038/nature04209 }}
*{{cite journal | author=Hofmann I, Thompson A, Sanderson CM, Munro S |title=The Arl4 family of small G proteins can recruit the cytohesin Arf6 exchange factors to the plasma membrane. |journal=Curr. Biol. |volume=17 |issue= 8 |pages= 711-6 |year= 2007 |pmid= 17398095 |doi= 10.1016/j.cub.2007.03.007 }}
}}
{{refend}}
{{refend}}


{{protein-stub}}
 
{{WikiDoc Sources}}
[[Category:Genes mutated in mice]]

Latest revision as of 18:15, 29 August 2017

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

n/a

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RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

ADP-ribosylation factor-like protein 4D is a protein that in humans is encoded by the ARL4D gene.[1][2]

Function

ADP-ribosylation factor 4D is a member of the ADP-ribosylation factor family of GTP-binding proteins. ARL4D is closely similar to ARL4A and ARL4C and each has a nuclear localization signal and an unusually high guanine nucleotide exchange rate. This protein may play a role in membrane-associated intracellular trafficking. Mutations in this gene have been associated with Bardet–Biedl syndrome (BBS).[2]

Model organisms

Model organisms have been used in the study of ARL4D function. A conditional knockout mouse line, called Arl4dtm1a(EUCOMM)Wtsi[11][12] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[13][14][15]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[9][16] Twenty five tests were carried out on mutant mice and significant abnormalities were observed.[9] Homozygous mutant females had decreased bone mineral content, heart weight, lean body mass and CD8-positive, alpha-beta memory T cell number. Males had abnormal rib morphology with vertebral transformation. Both sexes displayed a reduction in dorsal third ventricle area and hippocampal area.[9]

References

  1. ↑ Smith SA, Holik PR, Stevens J, Melis R, White R, Albertsen H (Jul 1995). "Isolation and mapping of a gene encoding a novel human ADP-ribosylation factor on chromosome 17q12-q21". Genomics. 28 (1): 113–5. doi:10.1006/geno.1995.1115. PMID 7590735.
  2. ↑ 2.0 2.1 "Entrez Gene: ARL4D ADP-ribosylation factor-like 4D".
  3. ↑ "DEXA data for Arl4d". Wellcome Trust Sanger Institute.
  4. ↑ "Radiography data for Arl4d". Wellcome Trust Sanger Institute.
  5. ↑ "Peripheral blood lymphocytes data for Arl4d". Wellcome Trust Sanger Institute.
  6. ↑ "Heart weight data for Arl4d". Wellcome Trust Sanger Institute.
  7. ↑ "Salmonella infection data for Arl4d". Wellcome Trust Sanger Institute.
  8. ↑ "Citrobacter infection data for Arl4d". Wellcome Trust Sanger Institute.
  9. ↑ 9.0 9.1 9.2 9.3 Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x.
  10. ↑ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  11. ↑ "International Knockout Mouse Consortium".
  12. ↑ "Mouse Genome Informatics".
  13. ↑ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  14. ↑ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  15. ↑ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  16. ↑ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.

External links

Further reading

  • Miki Y, Swensen J, Shattuck-Eidens D, Futreal PA, Harshman K, Tavtigian S, Liu Q, Cochran C, Bennett LM, Ding W (Oct 1994). "A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1". Science. 266 (5182): 66–71. doi:10.1126/science.7545954. PMID 7545954.
  • Harshman K, Bell R, Rosenthal J, Katcher H, Miki Y, Swenson J, Gholami Z, Frye C, Ding W, Dayananth P (Aug 1995). "Comparison of the positional cloning methods used to isolate the BRCA1 gene". Human Molecular Genetics. 4 (8): 1259–66. doi:10.1093/hmg/4.8.1259. PMID 7581362.
  • Bonaldo MF, Lennon G, Soares MB (Sep 1996). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome Research. 6 (9): 791–806. doi:10.1101/gr.6.9.791. PMID 8889548.
  • Jacobs S, Schilf C, Fliegert F, Koling S, Weber Y, Schürmann A, Joost HG (Aug 1999). "ADP-ribosylation factor (ARF)-like 4, 6, and 7 represent a subgroup of the ARF family characterization by rapid nucleotide exchange and a nuclear localization signal". FEBS Letters. 456 (3): 384–8. doi:10.1016/S0014-5793(99)00759-0. PMID 10462049.
  • Ingley E, Williams JH, Walker CE, Tsai S, Colley S, Sayer MS, Tilbrook PA, Sarna M, Beaumont JG, Klinken SP (Oct 1999). "A novel ADP-ribosylation like factor (ARL-6), interacts with the protein-conducting channel SEC61beta subunit". FEBS Letters. 459 (1): 69–74. doi:10.1016/S0014-5793(99)01188-6. PMID 10508919.
  • Nonaka Y, Tsuda N, Shichijo S, Ito M, Maeda Y, Harada M, Kamura T, Shigemori M, Itoh K (Oct 2002). "Recognition of ADP-ribosylation factor 4-like by HLA-A2-restricted and tumor-reactive cytotoxic T lymphocytes from patients with brain tumors". Tissue Antigens. 60 (4): 319–27. doi:10.1034/j.1399-0039.2002.600406.x. PMID 12472661.
  • Chiang AP, Nishimura D, Searby C, Elbedour K, Carmi R, Ferguson AL, Secrist J, Braun T, Casavant T, Stone EM, Sheffield VC (Sep 2004). "Comparative genomic analysis identifies an ADP-ribosylation factor-like gene as the cause of Bardet-Biedl syndrome (BBS3)". American Journal of Human Genetics. 75 (3): 475–84. doi:10.1086/423903. PMC 1182025. PMID 15258860.
  • Fan Y, Esmail MA, Ansley SJ, Blacque OE, Boroevich K, Ross AJ, Moore SJ, Badano JL, May-Simera H, Compton DS, Green JS, Lewis RA, van Haelst MM, Parfrey PS, Baillie DL, Beales PL, Katsanis N, Davidson WS, Leroux MR (Sep 2004). "Mutations in a member of the Ras superfamily of small GTP-binding proteins causes Bardet-Biedl syndrome". Nature Genetics. 36 (9): 989–93. doi:10.1038/ng1414. PMID 15314642.
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