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{{PBB|geneid=117531}}
{{PBB|geneid=117531}}
'''Transmembrane channel-like protein 1''' is a [[protein]] that in humans is encoded by the ''TMC1'' [[gene]].<ref name="pmid11850618">{{cite journal | author = Kurima K, Peters LM, Yang Y, Riazuddin S, Ahmed ZM, Naz S, Arnaud D, Drury S, Mo J, Makishima T, Ghosh M, Menon PS, Deshmukh D, Oddoux C, Ostrer H, Khan S, Riazuddin S, Deininger PL, Hampton LL, Sullivan SL, Battey JF Jr, Keats BJ, Wilcox ER, Friedman TB, Griffith AJ | title = Dominant and recessive deafness caused by mutations of a novel gene, TMC1, required for cochlear hair-cell function | journal = Nat Genet | volume = 30 | issue = 3 | pages = 277–84 |date=Mar 2002 | pmid = 11850618 | pmc = | doi = 10.1038/ng842 }}</ref><ref name="pmid11850623">{{cite journal | author = Vreugde S, Erven A, Kros CJ, Marcotti W, Fuchs H, Kurima K, Wilcox ER, Friedman TB, Griffith AJ, Balling R, Hrabe De Angelis M, Avraham KB, Steel KP | title = Beethoven, a mouse model for dominant, progressive hearing loss DFNA36 | journal = Nat Genet | volume = 30 | issue = 3 | pages = 257–8 |date=Mar 2002 | pmid = 11850623 | pmc = | doi = 10.1038/ng848 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: TMC1 transmembrane channel-like 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=117531| accessdate = }}</ref> TMC1 contains six transmembrane domains with both the C and N termini on the endoplasmic side of the membrane, as well as a large loop between domains 4 and 5. This topology is similar to that of [[transient receptor potential channels]] (TRPs), <ref>{{cite pmid|11850618}}</ref> a family of proteins involved in the perception of senses such as temperature, taste, pressure, and vision. <ref>{{cite pmid|25053448}}</ref> TMC1 has been located in the post-natal mouse choclea,<ref>{{cite pmid|11850618}}</ref> and knockouts for TMC1 and [[TMC2]] result in both auditory and vestibular deficits indicating TMC1 is a molecular part of auditory trasduction <ref>{{cite pmid|22105175}}</ref>
'''Transmembrane channel-like protein 1''' is a [[protein]] that in humans is encoded by the ''TMC1'' [[gene]].<ref name="Kurima_2002">{{cite journal | author = Kurima K, Peters LM, Yang Y, Riazuddin S, Ahmed ZM, Naz S, Arnaud D, Drury S, Mo J, Makishima T, Ghosh M, Menon PS, Deshmukh D, Oddoux C, Ostrer H, Khan S, Riazuddin S, Deininger PL, Hampton LL, Sullivan SL, Battey JF, Keats BJ, Wilcox ER, Friedman TB, Griffith AJ | title = Dominant and recessive deafness caused by mutations of a novel gene, TMC1, required for cochlear hair-cell function | journal = Nat Genet | volume = 30 | issue = 3 | pages = 277–84 | date = Mar 2002 | pmid = 11850618 | pmc = | doi = 10.1038/ng842 }}</ref><ref name="Vreugde_2002">{{cite journal | author = Vreugde S, Erven A, Kros CJ, Marcotti W, Fuchs H, Kurima K, Wilcox ER, Friedman TB, Griffith AJ, Balling R, Hrabé De Angelis M, Avraham KB, Steel KP | title = Beethoven, a mouse model for dominant, progressive hearing loss DFNA36 | journal = Nat Genet | volume = 30 | issue = 3 | pages = 257–8 | year = 2002 | pmid = 11850623 | pmc = | doi = 10.1038/ng848 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: TMC1 transmembrane channel-like 1| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=117531| accessdate = }}</ref> TMC1 contains six transmembrane domains with both the C and N termini on the endoplasmic side of the membrane, as well as a large loop between domains 4 and 5. This topology is similar to that of [[transient receptor potential channels]] (TRPs),<ref name="Kurima_2002"/> a family of proteins involved in the perception of senses such as temperature, taste, pressure, and vision.<ref>{{cite journal | author = Vriens J, Nilius B, Voets T | title = Peripheral thermosensation in mammals | journal = Nature Reviews Neuroscience | volume = 15 | issue = 9 | pages = 573-89 | year = 2014 | pmid = 25053448 | doi = 10.1038/nrn3784 }}</ref> TMC1 has been located in the post-natal mouse choclea,<ref name="Kurima_2002"/> and knockouts for TMC1 and [[TMC2]] result in both auditory and vestibular deficits indicating TMC1 is a molecular part of auditory trasduction.<ref name="pmid22105175">{{cite journal | author = Kawashima Y, Géléoc GS, Kurima K, Labay V, Lelli A, Asai Y, Makishima T, Wu DK, Della Santina CC, Holt JR, Griffith AJ | title = Mechanotransduction in mouse inner ear hair cells requires transmembrane channel-like genes | journal = J. Clin. Invest. | volume = 121 | issue = 12 | pages = 4796–809 | year = 2011 | pmid = 22105175 | pmc = 3223072 | doi = 10.1172/JCI60405 }}</ref>


== Function ==
== Function ==


This gene is considered a member of a gene family predicted to encode [[transmembrane]] proteins. Until recently, the specific function of this gene was relatively unknown; it was only known to be required for normal function of [[hair cell|cochlear hair cells]].<ref name="entrez"/> However, new research suggests that TMC1 interacts with [[Tip link]] proteins [[PCDH15|protocadherin 15]] and [[CDH23|cadherin 23]] indicating that TMC1, along with [[TMC2]], are necessary proteins for [[hair cell]] mechanotransduction. <ref>{{cite pmid|25114259}}</ref> Specifically, TMC1 and [[TMC2]] may be two pore-forming subunits of the channel that responds to tip link deflection in hair cells <ref>{{cite pmid| 23871232}}</ref>
This gene is considered a member of a gene family predicted to encode [[transmembrane]] proteins. Until recently, the specific function of this gene was relatively unknown; it was only known to be required for normal function of [[hair cell|cochlear hair cells]].<ref name="entrez"/> However, new research suggests that TMC1 interacts with [[Tip link]] proteins [[PCDH15|protocadherin 15]] and [[CDH23|cadherin 23]] indicating that TMC1, along with [[TMC2]], are necessary proteins for [[hair cell]] mechanotransduction.<ref name="Maeda_2014">{{cite journal | author = Maeda R, Kindt KS, Mo W, Morgan CP, Erickson T, Zhao H, Clemens-Grisham R, Barr-Gillespie PG, Nicolson T | title = Tip-link protein protocadherin 15 interacts with transmembrane channel-like proteins TMC1 and TMC2 | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 111 | issue = 35 | pages = 12907–12 | year = 2014 | pmid = 25114259 | doi = 10.1073/pnas.1402152111 }}</ref> Specifically, TMC1 and [[TMC2]] may be two pore-forming subunits of the channel that responds to tip link deflection in hair cells.<ref name="pmid23871232">{{cite journal | author = Pan B, Géléoc GS, Asai Y, Horwitz GC, Kurima K, Ishikawa K, Kawashima Y, Griffith AJ, Holt JR | title = TMC1 and TMC2 are components of the mechanotransduction channel in hair cells of the mammalian inner ear | journal = Neuron | volume = 79 | issue = 3 | pages = 504–15 | year = 2013 | pmid = 23871232 | pmc = 3827726 | doi = 10.1016/j.neuron.2013.06.019 }}</ref>


Due to its implication in choclear hair cell function and its interaction with hair cell tip links, TMC1 is being mutated and manipulated in order to better understand the receptor while at the same time producing a molecular model for deafness. While deafness can arise at any stage of auditory processing, DFNA36 (a type of progressive hearing loss) and DFNB7/B11 (congenital hearing loss) have been specifically shown to arise from TMC1 mutations. DFNA36 results from a dominant missense mutation and DFNB7/B11 results from a recessive mutation <ref>{{cite pmid|11850618}}</ref>. Both have been modeled in mice, known as the Beethoven model and the dn model respectively <ref>{{cite pmid|11850623}}</ref>. The TMC1 gene is located on [[chromosome]] 9q31-q21, and the dominant mutation associated with DFNA36 occurs at amino acid 572 <ref>{{cite pmid|17250663}}</ref>, which suggests the importance of this amino acid in the overall function of TMC1. Now that TMC1 has been shown to interact with the tip link proteins PCDH15 and CDH23<ref>{{cite pmid|25114259}}</ref>, the next question may be whether or not amino acid 572 is necessary for TMC1 tip link interactions.
Due to its implication in choclear hair cell function and its interaction with hair cell tip links, TMC1 is being mutated and manipulated in order to better understand the receptor while at the same time producing a molecular model for deafness. While deafness can arise at any stage of auditory processing, DFNA36 (a type of progressive hearing loss) and DFNB7/B11 (congenital hearing loss) have been specifically shown to arise from TMC1 mutations. DFNA36 results from a dominant missense mutation and DFNB7/B11 results from a recessive mutation.<ref name="Kurima_2002"/> Both have been modeled in mice, known as the Beethoven model and the dn model respectively.<ref name="Vreugde_2002"/> The TMC1 gene is located on [[chromosome]] 9q31-q21, and the dominant mutation associated with DFNA36 occurs at amino acid 572<ref name="Kitajiri_2007">{{cite journal | author = Kitajiri S, Makishima T, Friedman TB, Griffith AJ | title = A novel mutation at the DFNA36 hearing loss locus reveals a critical function and potential genotype-phenotype correlation for amino acid-572 of TMC1 | journal = Clin. Genet. | volume = 71 | issue = 2 | pages = 148–52 | year = 2007 | pmid = 17250663 | doi = 10.1111/j.1399-0004.2007.00739.x }}</ref> which suggests the importance of this amino acid in the overall function of TMC1. Now that TMC1 has been shown to interact with the tip link proteins PCDH15 and CDH23,<ref name="Maeda_2014"/> the next question may be whether or not amino acid 572 is necessary for TMC1 tip link interactions.


== Clinical significance ==
== Clinical significance ==


Mutations in this gene have been associated with progressive [[post-lingual deafness|postlingual hearing loss]], {{SWL|type=mutations_associated_to|target=Non-syndromic deafness|label=non syndromic deafness}}<ref>{{Cite pmid|24926664}}</ref> and profound [[prelingual deafness]].<ref name="entrez"/> TMC1 mutations are not associated with other symptoms or abnormalities, which is known as [[Nonsyndromic hearing loss]] and indicates that TMC1 functions mainly in auditory sensation. <ref>{{cite| pmid22652773}</ref> Additionally, recessive mutations of the gene result in both a loss of TMC1 function as well as profound deafness <ref>{{cite pmid|17250663}}</ref> indicating TMC1 function is necessary for the processing of auditory signals.
Mutations in this gene have been associated with progressive [[post-lingual deafness|postlingual hearing loss]], {{SWL|type=mutations_associated_to|target=Non-syndromic deafness|label=non syndromic deafness}}<ref>{{cite journal | author = Riahi Z, Bonnet C, Zainine R, Louha M, Bouyacoub Y, Laroussi N, Chargui M, Kefi R, Jonard L, Dorboz I, Hardelin JP, Salah SB, Levilliers J, Weil D, McElreavey K, Boespflug OT, Besbes G, Abdelhak S, Petit C | title = Whole Exome Sequencing Identifies New Causative Mutations in Tunisian Families with Non-Syndromic Deafness | journal = PLoS ONE | volume = 9 | issue = 6 | pages = e99797 | year = 2014 | pmid = 24926664 | doi = 10.1371/journal.pone.0099797 }}</ref> and profound [[prelingual deafness]].<ref name="entrez"/> TMC1 mutations are not associated with other symptoms or abnormalities, which is known as [[Nonsyndromic hearing loss]] and indicates that TMC1 functions mainly in auditory sensation.<ref name="pmid22652773">{{cite journal | author = Duman D, Tekin M | title = Autosomal recessive nonsyndromic deafness genes: a review | journal = Front Biosci (Landmark Ed) | volume = 17 | issue = | pages = 2213–36 | year = 2012 | pmid = 22652773 | pmc = 3683827 | doi = }}</ref> Additionally, recessive mutations of the gene result in both a loss of TMC1 function as well as profound deafness<ref name="Kitajiri_2007"/> indicating TMC1 function is necessary for the processing of auditory signals.




==References==
==References==
{{reflist}}
{{reflist|35em}}


==Further reading==
==Further reading==
{{refbegin | 2}}
{{refbegin|35em}}
*{{cite journal | author=Kitajiri SI, McNamara R, Makishima T, ''et al.'' |title=Identities, frequencies and origins of TMC1 mutations causing DFNB7/B11 deafness in Pakistan. |journal=Clin. Genet. |volume=72 |issue= 6 |pages= 546–50 |year= 2008 |pmid= 17877751 |doi= 10.1111/j.1399-0004.2007.00895.x }}
*{{cite journal | author = Kitajiri SI, McNamara R, Makishima T, Husnain T, Zafar AU, Kittles RA, Ahmed ZM, Friedman TB, Riazuddin S, Griffith AJ | title = Identities, frequencies and origins of TMC1 mutations causing DFNB7/B11 deafness in Pakistan. | journal = Clin. Genet. | volume = 72 | issue = 6 | pages = 546–50 | year = 2008 | pmid = 17877751 | doi = 10.1111/j.1399-0004.2007.00895.x }}
*{{cite journal | author=Kalay E, Karaguzel A, Caylan R, ''et al.'' |title=Four novel TMC1 (DFNB7/DFNB11) mutations in Turkish patients with congenital autosomal recessive nonsyndromic hearing loss. |journal=Hum. Mutat. |volume=26 |issue= 6 |pages= 591 |year= 2006 |pmid= 16287143 |doi= 10.1002/humu.9384 }}
*{{cite journal | author = Kalay E, Karaguzel A, Caylan R, Heister A, Cremers FP, Cremers CW, Brunner HG, de Brouwer AP, Kremer H | title = Four novel TMC1 (DFNB7/DFNB11) mutations in Turkish patients with congenital autosomal recessive nonsyndromic hearing loss. | journal = Hum. Mutat. | volume = 26 | issue = 6 | pages = 591 | year = 2006 | pmid = 16287143 | doi = 10.1002/humu.9384 }}
*{{cite journal | author=Meyer CG, Gasmelseed NM, Mergani A, ''et al.'' |title=Novel TMC1 structural and splice variants associated with congenital nonsyndromic deafness in a Sudanese pedigree. |journal=Hum. Mutat. |volume=25 |issue= 1 |pages= 100 |year= 2006 |pmid= 15605408 |doi= 10.1002/humu.9302 }}
*{{cite journal | author = Meyer CG, Gasmelseed NM, Mergani A, Magzoub MM, Muntau B, Thye T, Horstmann RD | title = Novel TMC1 structural and splice variants associated with congenital nonsyndromic deafness in a Sudanese pedigree. | journal = Hum. Mutat. | volume = 25 | issue = 1 | pages = 100 | year = 2006 | pmid = 15605408 | doi = 10.1002/humu.9302 }}
*{{cite journal | author=Ota T, Suzuki Y, Nishikawa T, ''et al.'' |title=Complete sequencing and characterization of 21,243 full-length human cDNAs. |journal=Nat. Genet. |volume=36 |issue= 1 |pages= 40–5 |year= 2004 |pmid= 14702039 |doi= 10.1038/ng1285 }}
*{{cite journal | author = Keresztes G, Mutai H, Heller S | title = TMC and EVER genes belong to a larger novel family, the TMC gene family encoding transmembrane proteins. | journal = BMC Genomics | volume = 4 | pages = 24 | year = 2003 | pmid = 12812529 | pmc = 165604 | doi = 10.1186/1471-2164-4-24 }}
*{{cite journal | author=Keresztes G, Mutai H, Heller S |title=TMC and EVER genes belong to a larger novel family, the TMC gene family encoding transmembrane proteins. |journal=BMC Genomics |volume=4 |pages= 24 |year= 2003 |pmid= 12812529 |doi= 10.1186/1471-2164-4-24 | pmc=165604 }}
*{{cite journal | author = Scott DA, Carmi R, Elbedour K, Yosefsberg S, Stone EM, Sheffield VC | title = An autosomal recessive nonsyndromic-hearing-loss locus identified by DNA pooling using two inbred Bedouin kindreds. | journal = Am. J. Hum. Genet. | volume = 59 | issue = 2 | pages = 385–91 | year = 1996 | pmid = 8755925 | pmc = 1914732 | doi = }}
*{{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 | pmc=139241 }}
*{{cite journal | author = Jain PK, Fukushima K, Deshmukh D, Ramesh A, Thomas E, Lalwani AK, Kumar S, Plopis B, Skarka H, Srisailapathy CR | title = A human recessive neurosensory nonsyndromic hearing impairment locus is potential homologue of murine deafness (dn) locus. | journal = Hum. Mol. Genet. | volume = 4 | issue = 12 | pages = 2391–4 | year = 1996 | pmid = 8634715 | doi = 10.1093/hmg/4.12.2391 }}
*{{cite journal | author=Scott DA, Carmi R, Elbedour K, ''et al.'' |title=An autosomal recessive nonsyndromic-hearing-loss locus identified by DNA pooling using two inbred Bedouin kindreds. |journal=Am. J. Hum. Genet. |volume=59 |issue= 2 |pages= 385–91 |year= 1996 |pmid= 8755925 |doi= | pmc=1914732 }}
*{{cite journal | author=Jain PK, Fukushima K, Deshmukh D, ''et al.'' |title=A human recessive neurosensory nonsyndromic hearing impairment locus is potential homologue of murine deafness (dn) locus. |journal=Hum. Mol. Genet. |volume=4 |issue= 12 |pages= 2391–4 |year= 1996 |pmid= 8634715 |doi=10.1093/hmg/4.12.2391 }}
{{refend}}
{{refend}}


Revision as of 21:23, 19 December 2014

Template:PBB Transmembrane channel-like protein 1 is a protein that in humans is encoded by the TMC1 gene.[1][2][3] TMC1 contains six transmembrane domains with both the C and N termini on the endoplasmic side of the membrane, as well as a large loop between domains 4 and 5. This topology is similar to that of transient receptor potential channels (TRPs),[1] a family of proteins involved in the perception of senses such as temperature, taste, pressure, and vision.[4] TMC1 has been located in the post-natal mouse choclea,[1] and knockouts for TMC1 and TMC2 result in both auditory and vestibular deficits indicating TMC1 is a molecular part of auditory trasduction.[5]

Function

This gene is considered a member of a gene family predicted to encode transmembrane proteins. Until recently, the specific function of this gene was relatively unknown; it was only known to be required for normal function of cochlear hair cells.[3] However, new research suggests that TMC1 interacts with Tip link proteins protocadherin 15 and cadherin 23 indicating that TMC1, along with TMC2, are necessary proteins for hair cell mechanotransduction.[6] Specifically, TMC1 and TMC2 may be two pore-forming subunits of the channel that responds to tip link deflection in hair cells.[7]

Due to its implication in choclear hair cell function and its interaction with hair cell tip links, TMC1 is being mutated and manipulated in order to better understand the receptor while at the same time producing a molecular model for deafness. While deafness can arise at any stage of auditory processing, DFNA36 (a type of progressive hearing loss) and DFNB7/B11 (congenital hearing loss) have been specifically shown to arise from TMC1 mutations. DFNA36 results from a dominant missense mutation and DFNB7/B11 results from a recessive mutation.[1] Both have been modeled in mice, known as the Beethoven model and the dn model respectively.[2] The TMC1 gene is located on chromosome 9q31-q21, and the dominant mutation associated with DFNA36 occurs at amino acid 572[8] which suggests the importance of this amino acid in the overall function of TMC1. Now that TMC1 has been shown to interact with the tip link proteins PCDH15 and CDH23,[6] the next question may be whether or not amino acid 572 is necessary for TMC1 tip link interactions.

Clinical significance

Mutations in this gene have been associated with progressive postlingual hearing loss, Template:SWL[9] and profound prelingual deafness.[3] TMC1 mutations are not associated with other symptoms or abnormalities, which is known as Nonsyndromic hearing loss and indicates that TMC1 functions mainly in auditory sensation.[10] Additionally, recessive mutations of the gene result in both a loss of TMC1 function as well as profound deafness[8] indicating TMC1 function is necessary for the processing of auditory signals.


References

  1. ^ a b c d Kurima K, Peters LM, Yang Y, Riazuddin S, Ahmed ZM, Naz S, Arnaud D, Drury S, Mo J, Makishima T, Ghosh M, Menon PS, Deshmukh D, Oddoux C, Ostrer H, Khan S, Riazuddin S, Deininger PL, Hampton LL, Sullivan SL, Battey JF, Keats BJ, Wilcox ER, Friedman TB, Griffith AJ (Mar 2002). "Dominant and recessive deafness caused by mutations of a novel gene, TMC1, required for cochlear hair-cell function". Nat Genet. 30 (3): 277–84. doi:10.1038/ng842. PMID 11850618.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. ^ a b Vreugde S, Erven A, Kros CJ, Marcotti W, Fuchs H, Kurima K, Wilcox ER, Friedman TB, Griffith AJ, Balling R, Hrabé De Angelis M, Avraham KB, Steel KP (2002). "Beethoven, a mouse model for dominant, progressive hearing loss DFNA36". Nat Genet. 30 (3): 257–8. doi:10.1038/ng848. PMID 11850623.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ a b c "Entrez Gene: TMC1 transmembrane channel-like 1".
  4. ^ Vriens J, Nilius B, Voets T (2014). "Peripheral thermosensation in mammals". Nature Reviews Neuroscience. 15 (9): 573–89. doi:10.1038/nrn3784. PMID 25053448.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  5. ^ Kawashima Y, Géléoc GS, Kurima K, Labay V, Lelli A, Asai Y, Makishima T, Wu DK, Della Santina CC, Holt JR, Griffith AJ (2011). "Mechanotransduction in mouse inner ear hair cells requires transmembrane channel-like genes". J. Clin. Invest. 121 (12): 4796–809. doi:10.1172/JCI60405. PMC 3223072. PMID 22105175.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  6. ^ a b Maeda R, Kindt KS, Mo W, Morgan CP, Erickson T, Zhao H, Clemens-Grisham R, Barr-Gillespie PG, Nicolson T (2014). "Tip-link protein protocadherin 15 interacts with transmembrane channel-like proteins TMC1 and TMC2". Proc. Natl. Acad. Sci. U.S.A. 111 (35): 12907–12. doi:10.1073/pnas.1402152111. PMID 25114259.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  7. ^ Pan B, Géléoc GS, Asai Y, Horwitz GC, Kurima K, Ishikawa K, Kawashima Y, Griffith AJ, Holt JR (2013). "TMC1 and TMC2 are components of the mechanotransduction channel in hair cells of the mammalian inner ear". Neuron. 79 (3): 504–15. doi:10.1016/j.neuron.2013.06.019. PMC 3827726. PMID 23871232.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ a b Kitajiri S, Makishima T, Friedman TB, Griffith AJ (2007). "A novel mutation at the DFNA36 hearing loss locus reveals a critical function and potential genotype-phenotype correlation for amino acid-572 of TMC1". Clin. Genet. 71 (2): 148–52. doi:10.1111/j.1399-0004.2007.00739.x. PMID 17250663.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Riahi Z, Bonnet C, Zainine R, Louha M, Bouyacoub Y, Laroussi N, Chargui M, Kefi R, Jonard L, Dorboz I, Hardelin JP, Salah SB, Levilliers J, Weil D, McElreavey K, Boespflug OT, Besbes G, Abdelhak S, Petit C (2014). "Whole Exome Sequencing Identifies New Causative Mutations in Tunisian Families with Non-Syndromic Deafness". PLoS ONE. 9 (6): e99797. doi:10.1371/journal.pone.0099797. PMID 24926664.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  10. ^ Duman D, Tekin M (2012). "Autosomal recessive nonsyndromic deafness genes: a review". Front Biosci (Landmark Ed). 17: 2213–36. PMC 3683827. PMID 22652773.

Further reading

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