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Importing Wikidata short description: "Protein-coding gene in the species Homo sapiens" (Shortdesc helper) |
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{{Short description|Protein-coding gene in the species Homo sapiens}}
{{Infobox_gene}}
'''Teashirt homolog 3''' is a [[protein]] that in humans is encoded by the ''TSHZ3'' [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: TSHZ3 teashirt family zinc finger 3| url =
''Tshz3''-[[knockout mouse|knockout mice]] do not develop the respiratory rhythm generator ([[
''TSHZ3'' has been identified as a critical region for a syndrome associated with heterozygous deletions at 19q12-q13.11, which includes autism spectrum disorder (ASD) symptoms such autistic traits, speech disturbance and intellectual disability, as well as renal tract abnormalities. Mice with heterozygous ''Tshz3'' deletion (''Tshz3<sup>lacZ</sup>''<sup>/+</sup>) show enrichment of ASD-related gene orthologs in the cerebral cortex, functional alterations of corticostriatal circuitry and ASD-relevant behavioral abnormalities.
==References==▼
<ref name="pmid27668656">{{cite journal | vauthors = Caubit X, Gubellini P, Andrieux J, Roubertoux PL, Metwaly M, Jacq B, Fatmi A, Had-Aissouni L, Kwan KY, Salin P, Carlier M, Liedén A, Rudd E, Shinawi M, Vincent-Delorme C, Cuisset JM, Lemaitre MP, Abderrehamane F, Duban B, Lemaitre JF, Woolf AS, Bockenhauer D, Severac D, Dubois E, Zhu Y, Sestan N, Garratt AN, Kerkerian-Le LG, Fasano L | display-authors = 6 | title = TSHZ3 deletion causes an autism syndrome and defects in cortical projection neurons | journal = Nature Genetics | volume = 48 | issue = 11 | pages = 1359–1369 | date = November 2016 | pmid = 27668656 | pmc = 5083212 | doi = 10.1038/ng.3681 }}</ref>
Postnatal conditional deletion of ''Tshz3'' in mouse induces behavioral deficits mimicking ASD, as well as abnormalities in synaptic transmission and plasticity in the corticostriatal circuit. These changes are associated to dysregulation of the cortical expression of more than 1000 genes, in particular coding for synaptic components, half of which has human orthologues involved in ASD.<ref>{{cite journal | vauthors = Chabbert D, Caubit X, Roubertoux PL, Carlier M, Habermann B, Jacq B, Salin P, Metwaly M, Frahm C, Fatmi A, Garratt AN, Severac D, Dubois E, Kerkerian-Le Goff L, Fasano L, Gubellini P | display-authors = 6 | title = Postnatal Tshz3 Deletion Drives Altered Corticostriatal Function and Autism Spectrum Disorder-like Behavior | journal = Biological Psychiatry | volume = 86 | issue = 4 | pages = 274–285 | date = August 2019 | pmid = 31060802 | doi = 10.1016/j.biopsych.2019.03.974 | s2cid = 85532974 | doi-access = free }}</ref>
▲== References ==
{{reflist}}
== Further reading ==
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* {{cite journal
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* {{cite journal | vauthors = Wiemann S, Weil B, Wellenreuther R, Gassenhuber J, Glassl S, Ansorge W, Böcher M, Blöcker H, Bauersachs S, Blum H, Lauber J, Düsterhöft A, Beyer A, Köhrer K, Strack N, Mewes HW, Ottenwälder B, Obermaier B, Tampe J, Heubner D, Wambutt R, Korn B, Klein M, Poustka A | display-authors = 6 | title = Toward a catalog of human genes and proteins: sequencing and analysis of 500 novel complete protein coding human cDNAs | journal = Genome Research | volume = 11 | issue = 3 | pages = 422–35 | date = March 2001 | pmid = 11230166 | pmc = 311072 | doi = 10.1101/gr.GR1547R }}
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== External links ==
* {{PDBe-KB2|Q63HK5|Teashirt homolog 3}}
{{PDB Gallery|geneid=57616}}
{{Transcription factors|g2}}
{{gene-19-stub}}
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