TUBA1B

Last update 08 May 2025

Basic Info

Synonyms

Alpha-tubulin ubiquitous, Detyrosinated tubulin alpha-1B chain, K-ALPHA-1

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Introduction

Tubulin is the major constituent of microtubules, a cylinder consisting of laterally associated linear protofilaments composed of alpha- and beta-tubulin heterodimers (PubMed:34996871). Microtubules grow by the addition of GTP-tubulin dimers to the microtubule end, where a stabilizing cap forms (PubMed:34996871). Below the cap, tubulin dimers are in GDP-bound state, owing to GTPase activity of alpha-tubulin (PubMed:34996871).

100 Clinical Results associated with TUBA1B

100 Translational Medicine associated with TUBA1B

0 Patents (Medical) associated with TUBA1B

114

Literatures (Medical) associated with TUBA1B

01 Jul 2025·Journal of Hazardous Materials

Triclosan-mediated metabolic oxidative stress-triggered cytoskeletal alterations in zebrafish gills and intestine: An integrated biomolecular and NMR-based metabolomics study

Article

Author: Dar, Owias Iqbal ; Gao, Yanan ; Jia, Ai-Qun ; Wang, Peng ; Vinothkanna, Annadurai ; Chen, Ligang ; Ke, Xiaosu

Triclosan (TCS) is a common disinfectant in consumer products, raising concerns about its effects on aquatic life. This study assessed the accumulation and impact of TCS on zebrafish (Danio rerio) by examining histological, biochemical, and NMR-based metabolomic changes in gill and intestinal tissue after 30 d of exposure to environmental concentrations (30, 50, and 70 µg/L). Both tissues showed TCS accumulation, which resulted in histopathological damage. The activity of catalase, lactate dehydrogenase, and acetylcholinesterase increased, while superoxide dismutase and glutathione S-transferase declined. Conversely, the content of malondialdehyde rose, but soluble protein decreased. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis displayed a varied spectrum of protein profiles, demonstrating alterations in the cytoskeletal proteins. Fourier-transform infrared spectroscopy indicated concentration-dependent alterations in the cytoskeletal protein secondary structures. Gene expression studies revealed alterations in the mRNA expression of genes associated with oxidative stress (sod-Cu/Zn, cat and mgst3b), metabolism (ldha), neural activity (ache), and cytoskeletal dynamics (actn4, myl9a, tpma, tuba1b and desmb). Nuclear magnetic resonance spectroscopy revealed significant changes in metabolic pathway profiles, validated by amino acid analysis. These results suggest that TCS can disrupt aquatic ecosystems by inducing oxidative stress, affecting cytoskeletal dynamics, and modifying metabolic processes.

01 May 2025·Behavioural Brain Research

Neuroprotective effect of nano-carboxymethyl chitosan from Doryteuthis sibogae against rotenone-induced Parkinson’s disease in the zebrafish model

Article

Author: Vijayashree, R ; Ramachandran, Saravanan ; Palaniselvam, Srinivasan ; Narasimman, Vignesh

This study investigates the neuroprotective effects of N-carboxymethyl chitosan (N-CMC) against rotenone (ROT)-induced Parkinson's disease (PD) in a zebrafish (ZF) model. In vivo experiments revealed that ROT-exposed ZF larvae exhibited reduced locomotor activity, increased edge preference, and impaired touch response, while N-CMC treatment significantly improved these behavioral parameters. The reactive oxygen species (ROS) levels in ROT-exposed larvae were elevated (37.75 %) but decreased with N-CMC treatment (30.28 %). Apoptosis was also reduced from 38.87 % in ROT-exposed larvae to 16.52 % with N-CMC treatment. In vitro studies using the N2A cell line confirmed N-CMC's neuroprotective effects. In adult ZF, ROT exposure decreased locomotion, and N-CMC treatment reversed these effects, as demonstrated through ToxTrac analysis. Novel Tank and Light/Dark tests showed significant behavioral improvements with N-CMC. Neurotransmitter analysis indicated increased dopamine, GABA, and glutamate levels in ROT-exposed ZF, which were moderated with N-CMC treatment. Gene expression analysis of gap43, syn2a, and tuba1b showed upregulation in ROT-exposed ZF, while N-CMC treatment downregulated these genes. Antioxidant assays demonstrated that ROT decreased SOD, CAT, and GSH levels in the brain, while N-CMC treatment increased these antioxidant levels by 1.3-fold, 7.5-fold, and 1.3-fold, respectively. Histopathology revealed neuronal degeneration in ROT-exposed ZF brains, but N-CMC treatment protected the neuronal loss. This study is the first to explore the neuroprotective and antioxidant properties of N-CMC in a ZF model, indicating its potential therapeutic benefits over conventional ROT-based treatments for PD.

01 Mar 2025·Transplantation

Downregulation of Tumor Suppressor Gene LKB1 During Severe Primary Graft Dysfunction After Human Lung Transplantation: Implication for the Development of Chronic Lung Allograft Dysfunction

Article

Author: Bremner, Ross ; Mohanakumar, Thalachallour ; Eguchi, Natsuki ; Rahman, Mohammad ; Sankpal, Narendra V. ; Scozzi, Davide ; Fleming, Timothy ; Sureshbabu, Angara ; Hachem, Ramsey ; Klein, Rachel ; Smith, Michael

Background.Severe primary graft dysfunction (PGD) after lung transplantation (LTx) is a significant risk factor for the development of bronchiolitis obliterans syndrome (BOS). Recent data from our group demonstrated that small extracellular vesicles (sEVs) isolated from the plasma of LTx recipients with BOS have reduced levels of tumor suppressor gene liver kinase B1 (LKB1) and promote epithelial-to-mesenchymal transition (EMT) and fibrosis. Here, we hypothesized that early inflammatory responses associated with severe PGD (PGD2/3) can downregulate LKB1 levels in sEVs, predisposing to the development of chronic lung allograft dysfunction (CLAD).Methods.sEVs were isolated from the plasma of human participants by Exosome Isolation Kit followed by 0.20-µm filtration and characterized by NanoSight and immunoblotting analysis. Lung self-antigens (K alpha 1 tubulin, Collagen V), LKB1, nuclear factor kappa B, and EMT markers in sEVs were compared by densitometry analysis between PGD2/3 and no-PGD participants. Neutrophil-derived factors and hypoxia/reperfusion effects on LKB1 levels and EMT were analyzed in vitro using quantitative real-time polymerase chain reaction and Western blotting.Results.LKB1 was significantly downregulated in PGD2/3 sEVs compared with no-PGD sEVs. Within PGD2/3 participants, lower post-LTx LKB1 was associated with CLAD development. Hypoxia/reperfusion downregulates LKB1 and is associated with markers of EMT in vitro. Finally, lower LKB1 levels in PGD2/3 are associated with increased markers of EMT.Conclusions.Our results suggest that in post-LTx recipients with PGD2/3, downregulation of LKB1 protein levels in sEVs is associated with increased EMT markers and may result in the development of CLAD. Our results also suggest that ischemia/reperfusion injury during LTx may promote CLAD through the early downregulation of LKB1.

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TUBA1B

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