The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
Identity is verified. The requested target is the human WHRN gene (historically DFNB31, also KIAA1526), encoding whirlin, not a similarly named gene from another organism. Literature describes human whirlin as an approximately 907-amino-acid, multi-PDZ-domain protein encoded at chromosome 9q32–q34. Its reported architecture—two harmonin N-like/harmonin-homology domains, three PDZ domains, a proline-rich region, and a terminal PDZ-binding motif—agrees with the supplied UniProt Q9P202 and InterPro annotations. The evidence therefore concerns the correct Homo sapiens protein. (mathur2019ushersyndromeand pages 2-3, whatley2020ushersyndromegenetics pages 10-11)
WHRN is not an enzyme or transporter: it has no established catalytic reaction or transported substrate. Its primary function is that of a multivalent cytoskeletal scaffold/adaptor. In sensory hair cells, distinct whirlin isoforms organize (1) the stereociliary tip machinery controlling actin-bundle growth and (2) the transient ankle-link complex controlling hair-bundle cohesion and morphogenesis. In photoreceptors, N-terminal/full-length whirlin scaffolds the USH2 protein network at the periciliary membrane surrounding the connecting cilium. (mathur2019ushersyndromeand pages 8-9, mathur2019ushersyndromeand pages 6-8)
A major recent mechanistic development is the recognition that these assemblies behave as biomolecular condensates. The 2023 ankle-link study showed that multivalent WHRN–PDZD7–USH2A–ADGRV1 interactions drive liquid–liquid phase separation (LLPS), and that deafness-associated mutations can impair condensation. This substantially sharpens the older description of whirlin as merely a static scaffold. (wang2023temporalandspatial pages 11-12, wang2023temporalandspatial pages 1-2)
WHRN uses multiple promoters and alternative splicing to generate full-length, N-terminal, and C-terminal species. Full-length whirlin contains the complete HNL/HHD–PDZ1–PDZ2–HNL/HHD2–proline-rich–PDZ3–PDZ-binding-motif architecture. C-terminal whirlin, transcribed principally from the downstream region, lacks PDZ1 and PDZ2 but retains HNL2/HHD2, the proline-rich region, PDZ3, and the terminal motif. N-terminal species contain one or both of PDZ1 and PDZ2. Retina has evidence for full-length, N-terminal, and C-terminal transcripts, whereas full-length and C-terminal proteins are the principal species detected in inner-ear tissue. (mathur2019ushersyndromeand pages 2-3, mathur2019ushersyndromeand pages 3-5, mathur2019ushersyndromeand pages 5-6)
This isoform structure is functionally important. The N-terminal PDZ tandem provides binding and self-assembly valency needed for USH2 complexes at the stereociliary ankle and photoreceptor periciliary membrane. C-terminal sequences participate particularly in the MYO15A–EPS8 machinery at growing stereociliary tips. Accordingly, pathogenic variants need to be interpreted against the transcript and isoform they disrupt, rather than only against a single canonical coding sequence. (mathur2019ushersyndromeand pages 3-5, mathur2019ushersyndromeand pages 6-8)
| Molecular species or isoform | Defining domains | Principal localization | Binding partners or complex | Primary structural role | Strongest evidence |
|---|---|---|---|---|---|
| WHRN or whirlin overall | Two HNL or HHD domains, three PDZ domains, a proline-rich region, and a C-terminal PDZ-binding motif | Hair-cell stereocilia and the photoreceptor periciliary region | Multivalent cytoskeletal and Usher-protein assemblies | Non-enzymatic adaptor and scaffold, not an enzyme or transporter; no catalytic reaction or transported substrate is known | Domain mapping, interaction assays, mutant animals, and rescue experiments support a scaffold function (mathur2019ushersyndromeand pages 2-3, mathur2019ushersyndromeand pages 6-8, mathur2019ushersyndromeand pages 9-10) |
| Full-length whirlin | HHD1 or HNL1, PDZ1, PDZ2, HHD2 or HNL2, proline-rich region, PDZ3, and terminal PDZ-binding motif | Stereociliary base or ankle; inner and vestibular hair-cell tips; photoreceptor periciliary membrane complex | ADGRV1, USH2A or usherin, PDZD7, MYO15A, and EPS8 | Stabilizes ankle links and developing hair-bundle architecture, supports stereocilia elongation, and organizes the retinal USH2 complex | Isoform-specific localization and mouse mutants establish requirements for ankle-link stability, outer-hair-cell bundle organization, and retinal USH2-protein localization (mathur2019ushersyndromeand pages 3-5, mathur2019ushersyndromeand pages 6-8, mathur2019ushersyndromeand pages 9-10) |
| C-terminal whirlin | HHD2 or HNL2, proline-rich region, PDZ3, and terminal PDZ-binding motif; lacks PDZ1 and PDZ2 | Developing stereociliary tips, especially in outer hair cells, as well as inner and vestibular hair-cell tips | MYO15A, EPS8, p55 or MPP1, and CASK | Promotes actin-bundle elongation and controls stereocilia length at the growing tip | Isoform-specific mouse studies show that C-terminal whirlin contributes to stereocilia elongation and that loss of both major isoforms produces abnormally short stereocilia (mathur2019ushersyndromeand pages 5-6, mathur2019ushersyndromeand pages 6-8) |
| Whirlin–MYO15A–EPS8 tip complex | WHRN HHD1 binds the EPS8 whirlin-binding region; WHRN PDZ3 binds the MYO15A terminal PDZ-binding motif; EPS8 PTB also binds MYO15A | Tip-complex density of elongating stereocilia | WHRN, MYO15A, and EPS8; GPSM2 and Gαi can enlarge the assembly in tallest stereocilia | Forms a phase-separated condensate that concentrates actin regulators and enhances EPS8-dependent F-actin bundling and stereocilia elongation | Purified proteins produced dynamic, fusion-competent, FRAP-positive condensates; wild-type complexes generated actin bundles averaging 301 ± 21 nm, compared with 144 ± 7 nm for a condensation-defective deafness mutant (lin2021phaseseparationmediatedcondensation pages 5-6, lin2021phaseseparationmediatedcondensation pages 1-3, lin2021phaseseparationmediatedcondensation pages 8-9) |
| Ankle-link complex | Multivalent contacts among the WHRN N-terminal PDZ tandem, PDZD7 PDZ domains, and terminal PDZ-binding motifs of USH2A and ADGRV1 | Ankle or base region of developing cochlear stereocilia | WHRN, PDZD7, USH2A or usherin, and ADGRV1 or VLGR1 | Condenses and anchors transient interstereociliary ankle links, preserving bundle cohesion and staircase-like morphogenesis | Reconstitution, calorimetry, pull-down, co-sedimentation, droplet, mutation, and mouse-localization experiments demonstrated phase-separation-dependent assembly; pathogenic variants impaired binding, condensation, or localization (wang2023temporalandspatial pages 11-12, wang2023temporalandspatial pages 1-2) |
| Retinal periciliary membrane complex | Primarily full-length or N-terminal WHRN species containing PDZ1 and PDZ2 | Membrane region surrounding the photoreceptor connecting cilium between inner and outer segments | WHRN, USH2A or usherin, and ADGRV1; reported associations also include SANS and RPGRORF15 | Scaffolds and stabilizes the retinal USH2 network and probably supports periciliary organization and protein trafficking, although its precise operation remains unresolved | Co-localization and Whrn-mutant studies show that WHRN loss destabilizes or mislocalizes usherin and ADGRV1 and that loss of N-terminal or full-length species can cause progressive retinal degeneration (mathur2019ushersyndromeand pages 8-9, mathur2019ushersyndromeand pages 5-6, mathur2019ushersyndromeand pages 9-10) |
Table: Evidence-based summary of whirlin isoforms and the principal hair-cell and retinal complexes they organize. It distinguishes WHRN’s non-catalytic scaffold role from enzymatic or transport functions.
At elongating stereociliary tips, whirlin forms a complex with MYO15A and EPS8. Interaction mapping indicates that WHRN HHD1 binds the EPS8 whirlin-binding region; WHRN PDZ3 recognizes the terminal PDZ-binding motif of MYO15A; and the EPS8 PTB domain also engages MYO15A. MYO15A acts as an actin-based motor that delivers or retains the complex at stereociliary tips, whereas EPS8 supplies actin-regulatory activity. Whirlin’s role is to organize these components into a high-local-concentration tip-complex density rather than catalyze actin polymerization itself. (mathur2019ushersyndromeand pages 6-8, li2023liquidliquidphaseseparation pages 4-6, lin2021phaseseparationmediatedcondensation pages 1-3)
Lin and colleagues provided direct evidence that this complex phase-separates. GFP-whirlin formed spherical, fluorescence-recovering puncta in cells; purified full-length whirlin formed concentration-dependent droplets that fused and exchanged molecules with solution, while increased salt suppressed droplet formation. The short whirlin species lacking HHD1, PDZ1, and PDZ2 did not phase-separate efficiently, supporting a requirement for multivalent self-interaction. Addition of MYO15A and EPS8 lowered the condensation threshold and yielded dynamic droplets containing all three proteins. (lin2021phaseseparationmediatedcondensation pages 5-6, lin2021phaseseparationmediatedcondensation pages 4-5)
The condensate has a measurable cytoskeletal consequence. Reconstituted WHRN–MYO15A–EPS8 droplets concentrated F-actin and produced bundles averaging 301 ± 21 nm in thickness, with maxima near 570 nm. A condensation-defective deafness-associated MYO15A mutant produced bundles of only 144 ± 7 nm. Thus, condensation appears to enhance or spatially focus EPS8-dependent actin bundling, supporting elongation of the tallest stereocilia. (lin2021phaseseparationmediatedcondensation pages 1-3, lin2021phaseseparationmediatedcondensation pages 8-9)
At the basal “ankle” of developing stereocilia, full-length WHRN works with PDZD7, USH2A/usherin, and ADGRV1/VLGR1. USH2A and ADGRV1 are large membrane proteins whose cytoplasmic C-terminal PDZ-binding motifs engage the WHRN N-terminal PDZ tandem. WHRN and PDZD7 thereby link membrane-spanning ankle-link proteins into a cytoplasmic scaffold that supports transient interstereociliary connections, bundle cohesion, and staircase-like development. (mathur2019ushersyndromeand pages 5-6, mathur2019ushersyndromeand pages 6-8, wang2023temporalandspatial pages 1-2)
The most important recent study, Wang et al., published March 2023 in Nature Communications (DOI), combined isothermal titration calorimetry, pull-down and co-sedimentation assays, reconstituted droplets, mutation analysis, and mouse localization. WHRN–USH2A interactions nucleated condensation, after which PDZD7 and ADGRV1 were recruited to form a quaternary ankle-link condensate. Disrupting multivalency markedly reduced WHRN accumulation at the stereociliary ankle. (wang2023temporalandspatial pages 11-12, wang2023temporalandspatial pages 1-2)
Disease-associated substitutions illuminate the mechanism. ADGRV1 Y6236X removed its PDZ-binding motif and prevented normal WHRN binding; PDZD7 G103R abolished USH2A binding; and WHRN T110A weakened condensate assembly. WHRN A64D and R223H retained partner binding but impaired WHRN self-association and LLPS, showing that dimerization/oligomerization contributes independently to scaffold function. High ADGRV1 concentration inhibited phase separation, providing a plausible developmental mechanism for dissolution of transient ankle links after approximately postnatal day 12 in mice. (wang2023temporalandspatial pages 11-12)
These findings shift the functional model from a rigid protein chain to a developmentally regulated condensate: WHRN supplies both binding specificity and network valency, and pathogenic variants can cause disease by changing condensation even when pairwise binding is not completely abolished.
In cochlear and vestibular hair cells, localization is both isoform- and cell-type-dependent. Full-length WHRN is found at the stereociliary base/ankle in inner, outer, and vestibular hair cells. Full-length and C-terminal whirlin occur at developing inner-hair-cell and vestibular-hair-cell tips, whereas C-terminal whirlin predominates at outer-hair-cell tips. Some historical discrepancies reflect antibody specificity, developmental stage, and failure to distinguish isoforms. (mathur2019ushersyndromeand pages 3-5, mathur2019ushersyndromeand pages 5-6, mathur2019ushersyndromeand pages 6-8)
In retinal photoreceptors, full-length and probably N-terminal whirlin localize to the periciliary membrane complex, adjacent to the connecting cilium between inner and outer segments. There WHRN co-localizes with USH2A and ADGRV1 and helps stabilize their localization. The complex is generally thought to support periciliary architecture and trafficking of material toward the outer segment, although WHRN’s exact retinal operation remains less experimentally resolved than its hair-cell functions. (mathur2019ushersyndromeand pages 8-9, mathur2019ushersyndromeand pages 5-6, mathur2019ushersyndromeand pages 9-10)
Whirlin has also been reported in myelinated axons. Whrn-deficient mice exhibit paranodal decompaction, cytoskeletal disruption, and axonal swellings from two weeks to one year of age, suggesting a broader cytoskeletal-linker role. However, sciatic-nerve conduction remained near 30 m/s and was not significantly altered, and this extra-sensory function is less firmly established for human disease than the auditory and retinal roles. (james2013organizationandfunction pages 127-132)
WHRN participates in a structural network rather than a classical metabolic or receptor-signaling pathway. Its best-supported processes are:
WHRN therefore acts upstream of sensory transduction chiefly by building the structures that make transduction possible; it is not itself established as an ion channel, receptor, motor, or signal-generating enzyme.
Biallelic WHRN variants cause two principal recessive phenotypes:
A useful—but not absolute—model relates phenotype to isoform disruption. Variants in the 5′/N-terminal, full-length-specific region tend to cause USH2D because they remove the PDZ1/PDZ2-containing species required in retina while potentially sparing downstream C-terminal expression. Variants in the 3′ region that impair both full-length and C-terminal functions, including PDZ3-dependent tip machinery, tend to produce severe DFNB31. Exceptions and limited family numbers mean that variant-specific clinical interpretation remains necessary. (mathur2019ushersyndromeand pages 3-5, whatley2020ushersyndromegenetics pages 10-11)
Mouse models support this model. The C-terminally disrupted Whrnwi model has short stereocilia, profound hearing loss, and no comparable retinal degeneration; 5′-region models such as Whrnneo have moderate hearing loss and progressive retinal abnormalities. Both can show vestibular evoked-potential deficits even when overt circling or balance behavior is absent, implying that subclinical vestibular dysfunction may be missed in patients without formal testing. (mathur2019ushersyndromeand pages 3-5, mathur2019ushersyndromeand pages 9-10)
Human–mouse whirlin conservation is high—approximately 88% overall amino-acid identity and 94.4% identity across PDZ domains—supporting the mechanistic relevance of mouse studies, while not eliminating species-specific differences in retinal phenotype or therapeutic windows. (mathur2019ushersyndromeand pages 9-10)
WHRN is included in hereditary hearing-loss, retinal-dystrophy, and Usher-syndrome sequencing panels. Practical interpretation should determine whether each allele disrupts full-length-only exons, shared C-terminal exons, splice usage, or a specific interaction/condensation interface. A molecular WHRN diagnosis should trigger audiometry and, where appropriate, retinal examination/electroretinography and vestibular assessment—even when the presenting phenotype appears nonsyndromic—because retinal disease may emerge later and vestibular deficits may be occult. The rarity of reported families and isoform complexity make segregation analysis and careful pathogenicity classification particularly important. (whatley2020ushersyndromegenetics pages 10-11, mathur2019ushersyndromeand pages 9-10)
No approved therapy restores WHRN’s molecular function. Current care is supportive: hearing aids when residual hearing is usable, cochlear implantation for severe-to-profound loss, visual rehabilitation and surveillance for retinal degeneration, and genetic counseling for autosomal-recessive inheritance. These are implementations for the clinical consequences of WHRN deficiency, not WHRN-targeted molecular treatments.
AAV delivery of full-length whirlin has produced partial rescue in mouse models, including improved retinal protein localization/degeneration, stereociliary morphology, and aspects of auditory or vestibular function. Delivery route strongly influenced outcome: posterior semicircular-canal administration transduced approximately 36% of cochlear hair cells versus about 15% after round-window delivery and produced partial functional improvement, whereas some delivery conditions restored protein without restoring hearing. These findings indicate both biological rescue potential and a narrow requirement for adequate cell targeting and developmental timing. (mathur2019ushersyndromeand pages 9-10)
As of the recent literature assessed here, no WHRN-specific human gene-replacement trial was identified. The 2023–2024 translational landscape therefore remains preclinical for WHRN, despite broader clinical advances in gene therapy for other hereditary deafness genes. The distinction is important: success in another genetic deafness cannot be assumed to transfer directly to WHRN because multiple isoforms, two sensory organs, and developmental hair-bundle defects complicate dosing, construct choice, and treatment timing.
The strongest functional conclusion is that WHRN is a compartment-specific, multivalent scaffold whose isoforms organize cytoskeletal and membrane-protein condensates. This conclusion is supported by convergent interaction mapping, purified-protein reconstitution, FRAP and droplet-fusion behavior, pathogenic-mutant analysis, subcellular localization, mouse knockouts, and partial gene-replacement rescue. (lin2021phaseseparationmediatedcondensation pages 5-6, wang2023temporalandspatial pages 11-12, lin2021phaseseparationmediatedcondensation pages 1-3)
Three limitations remain important:
Human WHRN/Q9P202 encodes whirlin, a non-catalytic PDZ scaffold essential for the architecture of auditory and retinal sensory cells. Its best-defined actions occur at stereociliary tips, where it condenses MYO15A and EPS8 to promote actin-bundle growth, and at stereociliary ankles, where it condenses PDZD7, USH2A, and ADGRV1 to assemble transient lateral links. In photoreceptors, full-length/N-terminal whirlin stabilizes the USH2 complex at the periciliary membrane. Isoform-selective disruption explains much, though not all, of the distinction between nonsyndromic DFNB31 deafness and USH2D. Genetic diagnosis and sensory surveillance are current real-world applications; WHRN replacement remains promising but preclinical.
References
(mathur2019ushersyndromeand pages 2-3): Pranav Dinesh Mathur and Jun Yang. Usher syndrome and non-syndromic deafness: functions of different whirlin isoforms in the cochlea, vestibular organs, and retina. Hearing Research, 375:14-24, Apr 2019. URL: https://doi.org/10.1016/j.heares.2019.02.007, doi:10.1016/j.heares.2019.02.007. This article has 75 citations and is from a domain leading peer-reviewed journal.
(whatley2020ushersyndromegenetics pages 10-11): Meg Whatley, Abbie Francis, Zi Ying Ng, Xin Ee Khoh, Marcus D. Atlas, Rodney J. Dilley, and Elaine Y. M. Wong. Usher syndrome: genetics and molecular links of hearing loss and directions for therapy. Frontiers in Genetics, Oct 2020. URL: https://doi.org/10.3389/fgene.2020.565216, doi:10.3389/fgene.2020.565216. This article has 69 citations and is from a peer-reviewed journal.
(mathur2019ushersyndromeand pages 8-9): Pranav Dinesh Mathur and Jun Yang. Usher syndrome and non-syndromic deafness: functions of different whirlin isoforms in the cochlea, vestibular organs, and retina. Hearing Research, 375:14-24, Apr 2019. URL: https://doi.org/10.1016/j.heares.2019.02.007, doi:10.1016/j.heares.2019.02.007. This article has 75 citations and is from a domain leading peer-reviewed journal.
(mathur2019ushersyndromeand pages 6-8): Pranav Dinesh Mathur and Jun Yang. Usher syndrome and non-syndromic deafness: functions of different whirlin isoforms in the cochlea, vestibular organs, and retina. Hearing Research, 375:14-24, Apr 2019. URL: https://doi.org/10.1016/j.heares.2019.02.007, doi:10.1016/j.heares.2019.02.007. This article has 75 citations and is from a domain leading peer-reviewed journal.
(wang2023temporalandspatial pages 11-12): Huang Wang, Haibo Du, Rui Ren, Tingting Du, Lin Lin, Zhe Feng, Dange Zhao, Xiaoxi Wei, Xiaoyan Zhai, Hongyang Wang, Tingting Dong, Jin-Peng Sun, Hao Wu, Zhigang Xu, and Qing Lu. Temporal and spatial assembly of inner ear hair cell ankle link condensate through phase separation. Nature Communications, Mar 2023. URL: https://doi.org/10.1038/s41467-023-37267-5, doi:10.1038/s41467-023-37267-5. This article has 17 citations and is from a highest quality peer-reviewed journal.
(wang2023temporalandspatial pages 1-2): Huang Wang, Haibo Du, Rui Ren, Tingting Du, Lin Lin, Zhe Feng, Dange Zhao, Xiaoxi Wei, Xiaoyan Zhai, Hongyang Wang, Tingting Dong, Jin-Peng Sun, Hao Wu, Zhigang Xu, and Qing Lu. Temporal and spatial assembly of inner ear hair cell ankle link condensate through phase separation. Nature Communications, Mar 2023. URL: https://doi.org/10.1038/s41467-023-37267-5, doi:10.1038/s41467-023-37267-5. This article has 17 citations and is from a highest quality peer-reviewed journal.
(mathur2019ushersyndromeand pages 3-5): Pranav Dinesh Mathur and Jun Yang. Usher syndrome and non-syndromic deafness: functions of different whirlin isoforms in the cochlea, vestibular organs, and retina. Hearing Research, 375:14-24, Apr 2019. URL: https://doi.org/10.1016/j.heares.2019.02.007, doi:10.1016/j.heares.2019.02.007. This article has 75 citations and is from a domain leading peer-reviewed journal.
(mathur2019ushersyndromeand pages 5-6): Pranav Dinesh Mathur and Jun Yang. Usher syndrome and non-syndromic deafness: functions of different whirlin isoforms in the cochlea, vestibular organs, and retina. Hearing Research, 375:14-24, Apr 2019. URL: https://doi.org/10.1016/j.heares.2019.02.007, doi:10.1016/j.heares.2019.02.007. This article has 75 citations and is from a domain leading peer-reviewed journal.
(mathur2019ushersyndromeand pages 9-10): Pranav Dinesh Mathur and Jun Yang. Usher syndrome and non-syndromic deafness: functions of different whirlin isoforms in the cochlea, vestibular organs, and retina. Hearing Research, 375:14-24, Apr 2019. URL: https://doi.org/10.1016/j.heares.2019.02.007, doi:10.1016/j.heares.2019.02.007. This article has 75 citations and is from a domain leading peer-reviewed journal.
(lin2021phaseseparationmediatedcondensation pages 5-6): Lin Lin, Yingdong Shi, Mengli Wang, Chao Wang, Qing Lu, Jinwei Zhu, and Rong-guang Zhang. Phase separation-mediated condensation of whirlin-myo15-eps8 stereocilia tip complex. Cell reports, 34 8:108770, Feb 2021. URL: https://doi.org/10.1016/j.celrep.2021.108770, doi:10.1016/j.celrep.2021.108770. This article has 29 citations and is from a highest quality peer-reviewed journal.
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(lin2021phaseseparationmediatedcondensation pages 8-9): Lin Lin, Yingdong Shi, Mengli Wang, Chao Wang, Qing Lu, Jinwei Zhu, and Rong-guang Zhang. Phase separation-mediated condensation of whirlin-myo15-eps8 stereocilia tip complex. Cell reports, 34 8:108770, Feb 2021. URL: https://doi.org/10.1016/j.celrep.2021.108770, doi:10.1016/j.celrep.2021.108770. This article has 29 citations and is from a highest quality peer-reviewed journal.
(li2023liquidliquidphaseseparation pages 4-6): Jianchao Li. Liquid-liquid phase separation in hair cell stereocilia development and maintenance. Computational and Structural Biotechnology Journal, 21:1738-1745, Feb 2023. URL: https://doi.org/10.1016/j.csbj.2023.02.040, doi:10.1016/j.csbj.2023.02.040. This article has 3 citations and is from a peer-reviewed journal.
(lin2021phaseseparationmediatedcondensation pages 4-5): Lin Lin, Yingdong Shi, Mengli Wang, Chao Wang, Qing Lu, Jinwei Zhu, and Rong-guang Zhang. Phase separation-mediated condensation of whirlin-myo15-eps8 stereocilia tip complex. Cell reports, 34 8:108770, Feb 2021. URL: https://doi.org/10.1016/j.celrep.2021.108770, doi:10.1016/j.celrep.2021.108770. This article has 29 citations and is from a highest quality peer-reviewed journal.
(james2013organizationandfunction pages 127-132): James Green. Organization and function of molecular domains in myelinated neurons. Text, 2013. URL: https://doi.org/10.17615/qmcn-th07, doi:10.17615/qmcn-th07. This article has 0 citations and is from a peer-reviewed journal.