📰 "Disrupting VDAC1-tubulin interaction uncovers crosstalk between mitochondrial and microtubule functions with implication to cancer therapy"
https://doi.org/doi:10.1007/s00018-026-06206-0https://pubmed.ncbi.nlm.nih.gov/42026323/ #Microtubule
Disrupting VDAC1–tubulin interaction uncovers crosstalk between mitochondrial and microtubule functions with implication to cancer therapy - Cellular and Molecular Life Sciences
Tubulin, a key component of the microtubule (MT) cytoskeleton, interacts with the mitochondrial gatekeeper protein VDAC1. Using a peptide array, we identif
📰 "Endothelial adenosine A2A receptor activation-mediated Tau hyperphosphorylation leads to blood-brain barrier breakdown in a chronic methamphetamine mouse model"
https://doi.org/doi:10.3389/fmed.2026.1801011https://pubmed.ncbi.nlm.nih.gov/42023109/ #Microtubule
Frontiers | Endothelial adenosine A2A receptor activation-mediated Tau hyperphosphorylation leads to blood–brain barrier breakdown in a chronic methamphetamine mouse model
IntroductionMethamphetamine (METH), a psychostimulant, can cause the blood–brain barrier (BBB) breakdown through astrocyte endfeet swelling and endothelial c...
📰 "Targeting of MARK2, but not other MARKs, suppresses TNBC progression by inhibition of the mutant p53-driven signaling pathway"
https://doi.org/doi:10.1016/S1875-5364(26)61172-7https://pubmed.ncbi.nlm.nih.gov/42019995/ #Microtubule📰 "Microtubule organization and molecular architecture of ciliary basal bodies in multiciliated airway cells"
https://doi.org/doi:10.1016/j.cub.2026.03.064https://pubmed.ncbi.nlm.nih.gov/42019505/ #Microtubule📰 "Tau oligomerization induces nuclear lamina invagination and chromatin remodeling in Alzheimer's disease"
https://doi.org/doi:10.1007/s00401-026-03018-1https://pubmed.ncbi.nlm.nih.gov/42017968/ #Microtubule
Tau oligomerization induces nuclear lamina invagination and chromatin remodeling in Alzheimer’s disease - Acta Neuropathologica
The aggregation of the microtubule-associated protein tau into oligomeric complexes is strongly correlated with the onset and progression of neurodegeneration in Alzheimer’s disease (AD). Increasing evidence implicates nuclear membrane disruption in AD and related tauopathies; however, whether this is a cause or consequence of neurodegeneration remains unresolved. Here, we show that nuclear lamina disruption emerges at the early Braak stages, coinciding with the initial formation of pathological tau aggregates in post-mortem AD brain tissue. Using the tauopathy mouse model (P301S PS19), we demonstrate that oligomeric tau (oTau) directly binds to the Lamin B Receptor (LBR), inducing nuclear envelope invaginations as revealed by electron microscopy. These structural alterations are accompanied by chromatin remodeling and gene expression dysregulation. To dissect the underlying mechanism, we employed a light-inducible OptoTau system (4R1N Tau::mCherry::Cry2Olig) in human iPSC-derived neurons, enabling real-time visualization of tau aggregation dynamics. This system revealed selective recruitment of oTau to the nuclear envelope and direct interactions with LBR and Lamin B2, leading to nuclear deformation and activation of the protein translational stress response. Together, these findings identify nuclear membrane disruption as an early and potentially causative event in tau-mediated neurodegeneration, establishing a mechanistic link between tau oligomerization, nuclear stress, and chromatin remodeling. Targeting nuclear destabilization may offer new therapeutic avenues for mitigating AD pathogenesis.
📰 "Wdr62 and Patronin cooperate to organize distinct acentrosomal microtubule networks during Drosophila oogenesis"
https://www.biorxiv.org/content/10.64898/2026.04.19.719433v1?rss=1 #Microtubule📰 "Engineering quantum optical responses of microtubules through tryptophan-network simulations and ultraviolet spectroscopy"
https://arxiv.org/abs/2604.18604 #Physics.Bio-Ph
#Microtubule #Quant-Ph
Engineering quantum optical responses of microtubules through tryptophan-network simulations and ultraviolet spectroscopy
Microtubules host dense ultraviolet-absorbing aromatic networks, suggesting an opportunity to engineer their optical response for biotechnology. Here we assess the feasibility of tuning microtubule fluorescence by combining an excitonic radiative-coupling model with molecular-dynamics-derived microtubule-like assemblies and steady-state absorbance and fluorescence measurements in microplate geometries. Simulations quantify how positional and orientational fluctuations reshape radiative rates and quantum yield, and predict how perturbing the tryptophan network by removing a specific site, adding an extra tryptophan at candidate binding pockets, or using mixed modification fractions can modulate emission. Experiments on porcine tubulin dimers and taxol-stabilized microtubules support these trends: polymerization enhances microtubule quantum yield at 280 nm and yields bounded changes at 295 nm due to scattering, while added L-tryptophan reproducibly quenches microtubules at both wavelengths. Together, theory and experiment provide evidence for chemically addressable tuning of microtubule quantum yield and motivate design rules for engineered microtubule photonics.
📰 "Engineering quantum optical responses of microtubules through tryptophan-network simulations and ultraviolet spectroscopy"
https://arxiv.org/abs/2604.18604 #Physics.Bio-Ph
#Microtubule #Dynamics #Quant-Ph
Engineering quantum optical responses of microtubules through tryptophan-network simulations and ultraviolet spectroscopy
Microtubules host dense ultraviolet-absorbing aromatic networks, suggesting an opportunity to engineer their optical response for biotechnology. Here we assess the feasibility of tuning microtubule fluorescence by combining an excitonic radiative-coupling model with molecular-dynamics-derived microtubule-like assemblies and steady-state absorbance and fluorescence measurements in microplate geometries. Simulations quantify how positional and orientational fluctuations reshape radiative rates and quantum yield, and predict how perturbing the tryptophan network by removing a specific site, adding an extra tryptophan at candidate binding pockets, or using mixed modification fractions can modulate emission. Experiments on porcine tubulin dimers and taxol-stabilized microtubules support these trends: polymerization enhances microtubule quantum yield at 280 nm and yields bounded changes at 295 nm due to scattering, while added L-tryptophan reproducibly quenches microtubules at both wavelengths. Together, theory and experiment provide evidence for chemically addressable tuning of microtubule quantum yield and motivate design rules for engineered microtubule photonics.
Rxiv cytoskeleton
Rxiv mechanobio