ArticleJournal of the Association for Research in Otolaryngology : JARO2015
Hair Cell Loss, Spiral Ganglion Degeneration, and Progressive Sensorineural Hearing Loss in Mice with Targeted Deletion of Slc44a2/Ctl2.
Article in Journal of the Association for Research in Otolaryngology : JARO, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- SLC44A2 negatively regulates mitochondrial fatty acid oxidation to suppress colorectal progression by blocking the MUL1-CPT2 interaction.Cell death & disease · 2025Article
- SLC44A2 regulates vascular smooth muscle cell phenotypic switching and aortic aneurysm.The Journal of clinical investigation · 2024Article
- Lack of the human choline transporter-like protein SLC44A2 causes hearing impairment and a rare red blood phenotype.EMBO molecular medicine · 2023Article
- Platelet-Neutrophil Crosstalk in Thrombosis.International journal of molecular sciences · 2023Review
- Loss of the chromatin remodeler CHD7 impacts glial cells and myelination in the mouse cochlear spiral ganglion.Hearing research · 2022Article
- Downregulation of GJB2 and SLC26A4 genes induced by noise exposure is associated with cochlear damage.Molecular biology reports · 2022Article
- The Roles of Solute Carriers in Auditory Function.Frontiers in genetics · 2022Review
- Functional and Biochemical Consequences of Disease Variants in Neurotransmitter Transporters: A Special Emphasis on Folding and Trafficking Deficits.Pharmacology & therapeutics · 2021Review
- Characteristics of head and neck squamous cell carcinoma cell Lines reflect human tumor biology independent of primary etiologies and HPV status.Translational oncology · 2020Article
- The choline transporter Slc44a2 controls platelet activation and thrombosis by regulating mitochondrial function.Nature communications · 2020Article
- SLC44A2 deficient mice have a reduced response in stenosis but not in hypercoagulability driven venous thrombosis.Journal of thrombosis and haemostasis : JTH · 2020Article
- Dual AAV-mediated gene therapy restores hearing in a DFNB9 mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2.Thrombosis research · 2018Article
- SLC44A2 single nucleotide polymorphisms, isoforms, and expression: Association with severity of Meniere's disease?Genomics · 2016Article
- Noise exposure modulates cochlear inner hair cell ribbon volumes, correlating with changes in auditory measures in the FVB/nJ mouse.Scientific reports · 2016Article
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Authors and funding
20 authors at 2 institutions in 1 country.
Funding
Abstract
SLC44A2 (solute carrier 44a2), also known as CTL2 (choline transporter-like protein 2), is expressed in many supporting cell types in the cochlea and is implicated in hair cell survival and antibody-induced hearing loss. In mice with the mixed C57BL/6-129 background, homozygous deletion of Slc44a2 exons 3–10 (Slc44a2(Δ/Δ)resulted in high-frequency hearing loss and hair cell death. To reduce effects associated with age-related hearing loss (ARHL) in these strains, mice carrying the Slc44a2Δ allele were backcrossed to the ARHL-resistant FVB/NJ strain and evaluated after backcross seven(N7) (99 % FVB). Slc44a2(Δ/Δ) mice produced abnormally spliced Slc44a2 transcripts that contain a frame shift and premature stop codons. Neither full-length SLC44A2 nor a putative truncated protein could be detected in Slc44a2(Δ/Δ) mice, suggesting a likely null allele. Auditory brain stem responses (ABRs) of mice carrying the Slc44a2Δ allele on an FVB/NJ genetic background were tested longitudinally between the ages of 2 and 10 months. By 6 months of age,Slc44a2(Δ/Δ) mice exhibited hearing loss at 32 kHz,but at 12 and 24 kHz had sound thresholds similar to those of wild-type Slc44a2(+/+) and heterozygous +/Slc44a2Δ mice. After 6 months of age, Slc44a2(Δ/Δ) mutants exhibited progressive hearing loss at all frequencies and +/Slc44a2(Δ) mice exhibited moderate threshold elevations at high frequency. Histologic evaluation of Slc44a2(Δ/Δ) mice revealed extensive hair cell and spiral ganglion cell loss, especially in the basal turn of the cochlea. We conclude that Slc44a2 function is required for long-term hair cell survival and maintenance of hearing.
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