TSHZ3: Difference between revisions

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'''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 = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=57616| accessdate = }}</ref> In mice, it is a necessary part of the neural circuitry that controls breathing. The gene is also a homolog of the [[Drosophila melanogaster]] teashirt gene, which encodes a [[zinc finger]] [[transcription factor]] important for development of the trunk.
 
''Tshz3''-[[knockout mouse|knockout mice]] do not develop the respiratory rhythm generator ([[Central pattern generator#Rhythm generators|RRG]]) neural circuit, which is a pacemaker that produces an oscillating rhythm in the brainstem and controls autonomous breathing. The RRG [[neuron]]s are present, but are abnormal. Those mice do not survive because they don't initiate breathing after birth. Tshz-3''Tshz3'' is being studied for its relationship to infant breathing defects in humans.<ref name="pmid20631175">{{cite journal | vauthors = Caubit X, Thoby-Brisson M, Voituron N, Filippi P, Bévengut M, Faralli H, Zanella S, Fortin G, Hilaire G, Fasano L | title = Teashirt 3 regulates development of neurons involved in both respiratory rhythm and airflow control | journal = J. Neurosci. | volume = 30 | issue = 28 | pages = 9465–76 |date=July 2010 | pmid = 20631175 | doi = 10.1523/JNEUROSCI.1765-10.2010 | laysummary = https://www.newscientist.com/article/dn19218-single-gene-could-be-key-to-a-babys-first-breath.html | laysource = New Scientist }}</ref>
 
Recently, ''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.<ref>{{Cite web|url=https://www-ncbi-nlm-nih-gov.insb.bib.cnrs.fr/pubmed/?term=caubit+x|title=TSHZ3 deletion causes an autism syndrome and defects in cortical projection neurons.|last=|first=|date=|website=|archive-url=|archive-date=|dead-url=|access-date=}}</ref> 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.<ref>{{Cite web|url=https://www-ncbi-nlm-nih-gov.insb.bib.cnrs.fr/pubmed/?term=caubit+x|title=Login|website=www-ncbi-nlm-nih-gov.insb.bib.cnrs.fr|access-date=2018-01-31}}</ref>
 
==References==