Ask about this productRelated genes to: TUBB2b antibody
- Gene:
- TUBB2B NIH gene
- Name:
- tubulin beta 2B class IIb
- Previous symbol:
- -
- Synonyms:
- MGC8685, DKFZp566F223, bA506K6.1
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-03
- Date modifiied:
- 2015-12-17
Related products to: TUBB2b antibody
Related articles to: TUBB2b antibody
- Mammalian oocytes are filled with fibric structures called cytoplasmic lattice (CPL) that are essential for oocyte maturation and early embryonic development. CPL comprises subcortical maternal complex (SCMC) and multiple components, including PADI6. Although it was first discovered in the 1960s, the molecular architecture and assembly mechanisms of CPL remain poorly understood. Here we present the cryo-electron microscopy structure of CPL isolated from mouse oocytes. Our analysis identified 14 constitutive protein subunits and revealed that CPL is composed of repeating units comprising U-shaped basket (UB) and adapter ring (AR) features, forming a filamentous architecture. The AR adopts a two-fold symmetric conformation, containing two NLRP4F, four SCMC and two ZBED3 subunits circularized via two distinct interaction clusters. The UB is anchored by PADI6, a didecamer composed of ten homodimers assembled by two back-to-back pentamers, each forming the lateral side of the UB. The underfoot base and up and down sides of the UB are formed by multiple central-symmetric assemblies (UBE2D3-UHRF1-NLRP14) and (TUBB2B-TUBB2A-FBXW24-SKP1), respectively, associating with the PADI6 pentamers to construct the intact UB structure. Two SCMC dimers within each AR connect the up and down sides of two adjacent UBs with an extensive protein-protein interaction network, and thus maintain the repetitive connection between the neighbouring CPL units. Our work unveils the architectural principles underlying the assembly of this large, periodic CPL filament, offering a molecular basis for understanding the functions of CPL in early mammalian embryogenesis and female reproductive disorders. - Source: PubMed
Publication date: 2026/03/17
Liu ShuxianLiu YusongXue JunchaoLi ZhenzhenZhang YanLi BailunXu LidanLi LiliYu ZhenzhenYu HongtaoGao HaishanShen En-Zhi - Semantic variant of primary progressive aphasia is a clinical subtype of frontotemporal lobar degeneration and is marked by TDP-43 subtype C pathology (FTLD-TDP C). It is a sporadic disease, yet has a strikingly homogeneous clinicopathological presentation, suggesting a common pathophysiology. The aim of this study was to discover dysregulated pathways in FTLD-TDP C through transcriptomics of the temporal cortex, its most affected region. Bulk RNA sequencing was conducted on temporal cortices of a post-mortem cohort of 18 FTLD-TDP C patients and 23 sex- and age-matched controls. Differential expression and functional analyses were run to detect differentially expressed genes with FDR<0.05 (DEG) and functionally annotate them. We assessed enrichment of TARDBP's protein interactors and RNA targets in DEG. Our findings were compared to other published RNA sequencing data of tauopathies (Alzheimer's dementia, progressive supranuclear palsy and FTLD with MAPT), FTLD-TDP (subtypes A&B) and available proteomics of this cohort. Furthermore, we performed weighted gene co-expression network analysis (WGCNA). We adjusted for differences in cell type composition between cases and controls using cell deconvolution, and removed genes dysregulated in temporal cortices of other datasets. In DEG of FTLD-TDP we focused on enrichment of synaptic processes using SynGO. We found upregulation of damage response, cell structure, RNA splicing processes and downregulation of synaptic processes in 6322 DEG and five disease-related WGCNA modules. TARDBP-related genes were enriched in DEG. Additionally, transmembrane transport across the neurovascular unit was dysregulated. After cell deconvolution and removal of common tau-genes, postsynaptic processes remained dysregulated, specifically gene ontology terms 'modulation of chemical synaptic transmission' and 'neurotransmitter receptor localisation to postsynaptic specialisation membrane'. We found eleven synaptic FTLD-TDP C-specific genes affected on both RNA- and protein-level in the temporal cortex, which were involved in synaptic adhesion (CADM1, NCAN), signal transmission (COMT, RGS144, SLC1A2, TUBB2B) and synaptic plasticity (BEGAIN, ITPKA, LRFN1, RAB3B, SYNPO). In conclusion, a wide range of processes were dysregulated on RNA-level in the temporal cortex of FTLD-TDP C, including commonly affected processes in neurodegeneration, such as structural cell alterations. Dysregulation of TARDBP-related genes and RNA splicing has also been observed in other TDP-43 proteinopathies. Importantly, we found that postsynaptic processes were downregulated in FTLD-TDP C, after removing tauopathy-related genes and after cell deconvolution. In particular, assembly of receptors at the postsynaptic membrane and synaptic signal transmission were affected, both on RNA and protein level. Future research on these pathways could elucidate distinct pathophysiological mechanisms and guide targeted clinical approaches. - Source: PubMed
Publication date: 2026/03/06
Rajicic AnaMol Merel OMelhem ShamiramKisic Helenavan Swieten John CSeelaar Harrovan Rooij Jeroen G J - Nonsense-mediated mRNA decay (NMD) is associated with neurodevelopmental disorders, yet its role in cortical organization is unknown. We demonstrate that NMD mediated by UPF2 is indispensable for cortical organization. Conditional deletion of Upf2 in radial glial cells delays neuronal migration and disrupts cortical lamination. Trp53 knockout rescues microcephaly from Upf2 deficiency but cannot rescue lamination defects, showing that UPF2's role in neuronal migration is uncoupled from its regulation of cell cycle and independent of p53. UPF2 deficiency downregulates key neuronal migration genes in the Reelin signaling pathway and microtubule assembly (e.g., Dab1, Lrp8, Tubb2b, and Tuba1a), partly through upregulation of the transcriptional repressor Ino80. Additionally, NMD inhibition induces widespread upregulation of ciliary genes. Ectopic expression of Foxj1, a master regulator of ciliary genes and an NMD target, impedes neuronal migration, phenocopying Upf2 loss. Therefore, NMD is a central post-transcriptional mechanism coordinating migration and ciliary gene networks crucial for cortical structure development. - Source: PubMed
Publication date: 2026/02/25
Lin LinKubota NaotoLam Yi-LiSong Michelle MingxueZhang MinZheng Sika - Diethylhexyl phthalate (DEHP), a common plasticizer, has been associated with hormone disruption and carcinogenesis, but its molecular impact on uterine corpus endometrial carcinoma (UCEC) remains unclear. This study aims to computationally identify a gene signature based on known DEHP-associated toxic targets and evaluates their clinical and immunological relevance in UCEC. DEGs were intersected with DEHP targets from CTD and TargetNet databases. PPI networks, functional enrichment, and survival analyses were conducted. Prognostic genes were identified using Cox and LASSO regression. DEHP risk score models and nomograms were constructed. Immune infiltration was analyzed using ESTIMATE and ssGSEA algorithms. Molecular docking was performed via CB-Dock2. Seventy-five genetic targets linked to DEHP in toxicological databases were identified, and enrichment analyses revealed DEHP-related genes enriched in neurotransmission and hormone signaling pathways. Seven prognostic genes (HTR3A, GRM2, HTR6, THRB, TUBB2B, FOLH1, PGR) correlated with overall survival and histologic grade. The DEHP risk score effectively stratified patients. DEHP-THRB showed strongest binding affinity, suggesting direct toxicological interaction. This study characterizes a computationally derived gene signature associated with DEHP toxicity in UCEC, highlighting their prognostic and immunological significance as potential molecular footprints, while acknowledging that direct exposure inference requires future validation with measured biomonitoring data. - Source: PubMed
Publication date: 2026/01/30
Yin MinuoZhang Huimin - Age-related hearing loss (ARHL) is a prevalent neurodegenerative condition commonly linked to aging and chronic inflammation. However, there is currently a lack of substantial proteomic evidence elucidating the underlying mechanisms within the brain. - Source: PubMed
Publication date: 2026/01/07
Wang YanZhang ChanyuanMa XiaohuiZhao HeWang QiCui LimeiChen LiangSun Yan