Ask about this productRelated genes to: TMEM30B antibody
- Gene:
- TMEM30B NIH gene
- Name:
- transmembrane protein 30B
- Previous symbol:
- -
- Synonyms:
- CDC50B
- Chromosome:
- 14q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-17
- Date modifiied:
- 2018-12-07
Related products to: TMEM30B antibody
Related articles to: TMEM30B antibody
- The asymmetry of lipid membranes is tightly regulated in eukaryotic cells, and auditory hair cells are no exception. - Source: PubMed
Publication date: 2026/05/13
Park Yein ChristinaBallesteros Angela - Mechanotransduction within the cochlea depends on the precise architecture of hair bundles, yet our comprehension of the mechanisms that govern the formation and maintenance of the sound-receptive structure is still limited. Here, we identify Tmem30b, a phospholipid-flippase chaperone, as a critical regulator expressed in outer hair cells (OHCs). Although initially localized to the nuclear membrane at P5, Tmem30b translocates to and stabilizes within the stereocilia and the underlying cuticular plate during maturation. The mice exhibit an early-onset hearing loss with preserved vestibular and retinal functions. Notably, the disorganization of OHC stereocilia in mutants initiates at P7, coinciding with the initial presence of Tmem30b in stereocilia. Mechanistically, Tmem30b partners with Atp8b1 to regulate phospholipid asymmetry; disruption of this complex destabilizes OHC bundles. Crucially, AAV-mediated delivery of o hair cells alleviates stereocilia defects in both and mice. Furthermore, hair cell specific overexpression of Tmem30b protects mice from noise-induced and aminoglycoside-induced hearing loss. In summary, our findings establish Tmem30b as a pivotal organizer of OHC hair bundles and highlight Tmem30b-Atp8b1-mediated lipid regulation as a therapeutic target for hearing loss. - Source: PubMed
Publication date: 2026/04/29
Chang MiaoHong GuodongGao ShanCheng ChengYuan JiaXiao YuQiao RuifengKe JingWu XinhaoZhang TianchengGuo SiweiJiang RunzeLiu ZiyiZhou JingZhang XiaohanWu YunhaoZhao XiaoxuLi WenShen ShuyuanHe ZuhongBi XiuliChai RenjieFu Xiaolong - Sensory hair cells convert sound-induced vibrations into electrical signals through a process called mechanoelectrical transduction (MET). While the protein components of the MET complex are well studied, increasing evidence indicates that MET channel properties are significantly modulated by the surrounding lipid bilayer. The asymmetric distribution of membrane lipids between the inner and outer membrane leaflets is well established to shape membrane mechanics. The recent discovery that the core MET components TMC1 and TMC2 also act as lipid scramblases suggests a direct role for membrane lipid asymmetry in the dynamic shaping of auditory transduction. Because scramblase activity of TMC1/2 disrupts lipid asymmetry, we hypothesized that an opposing flippase may be required to restore and maintain lipid asymmetry. Here, we identify the P4-ATPase ATP8B1 and its chaperone TMEM30B as selectively expressed in outer hair cells (OHCs), enriched in stereocilia, and upregulated following the onset of MET and hearing. Loss of either protein results in elevated auditory brainstem response (ABR) thresholds, phosphatidylserine (PS) externalization, and rapid hair-cell degeneration, demonstrating that lipid homeostasis is crucial for OHC survival. Together, these findings establish ATP8B1 and TMEM30B as key regulators of membrane lipid asymmetry in sensory hair cells and establish TMEM30B as a novel deafness gene. - Source: PubMed
Publication date: 2026/02/13
De Hoyos Henry NLi SihanIm Jun-SubLuz-Ricca AlyssaSzeto BetsyJonas RachelKim EmmaAmin NikhilShin Jung-Bum - Odontoblasts are primarily responsible for synthesizing and secreting extracellular matrix proteins, which are crucial for dentinogenesis. Our previous single-cell profile and RNAscope for odontoblast lineage revealed that cyclic adenosine monophosphate responsive element-binding protein 3 like 1 (Creb3l1) was specifically enriched in the terminal differentiated odontoblasts. In this study, deletion of Creb3l1 in the Wnt1+ lineage led to insufficient root elongation and dentin deposition. Assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and RNA sequencing were performed to revealed that in CREB3L1-deficient mouse dental papilla cells (mDPCs), the genes near the closed chromatin regions were mainly associated with mesenchymal development and the downregulated genes were primarily related to biological processes including cell differentiation, protein biosynthesis and transport, all of which were evidenced by a diminished ability of odontoblastic differentiation, a significant reduction in intracellular proteins, and an even greater decline in extracellular supernatant proteins. Dentin matrix protein 1 (Dmp1), dentin sialophosphoprotein (Dspp), and transmembrane protein 30B (Tmem30b) were identified as direct transcriptional regulatory targets. TMEM30B was intensively expressed in the differentiated odontoblasts, and exhibited a significant decline in both CREB3L1-deficient odontoblasts in vivo and in vitro. Deletion of Tmem30b impaired the ability of odontoblastic differentiation, protein synthesis, and protein secretion in mDPCs. Moreover, overexpressing TMEM30B in CREB3L1-deficient mDPCs partially rescued the extracellular proteins secretion. Collectively, our findings suggest that CREB3L1 participates in dentinogenesis and facilitates odontoblastic differentiation by directly enhancing the transcription of Dmp1, Dspp, and other differentiation-related genes and indirectly promoting protein secretion partially via TMEM30B. - Source: PubMed
Publication date: 2024/10/10
Li YuanyuanLin YuxiuGuo JinqiangHuang DelanZuo HuanyanZhang HanshuYuan GuohuaLiu HuanChen Zhi - Patients who undergo gross total resection (GTR) of Central Nervous System World Health Organization (WHO) grade 1 meningioma constitute a "low-risk" group, but some low-risk meningiomas can recur despite reassuring clinical and histological features. In this study, gene expression values in newly diagnosed WHO grade 1 meningiomas that had undergone GTR were evaluated for their association with recurrence. - Source: PubMed
Publication date: 2024/08/05
Morshed Ramin ANguyen Minh PYoungblood Mark WPerlow Haley KLucas Calixto-Hope GPatel Akash JPalmer Joshua DChandler James PTheodosopoulos Philip VMagill Stephen TChen William CRaleigh David R