Ask about this productRelated genes to: MAP6 Blocking Peptide
- Gene:
- MAP6 NIH gene
- Name:
- microtubule associated protein 6
- Previous symbol:
- -
- Synonyms:
- KIAA1878, STOP, FLJ41346, MAP6-N
- Chromosome:
- 11q13.5
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-26
- Date modifiied:
- 2015-11-16
Related products to: MAP6 Blocking Peptide
Related articles to: MAP6 Blocking Peptide
- Understanding adaptive evolution has long fascinated evolutionary biologists. Adaptive phenotypic divergence is often driven by modifications to protein-coding sequences. The group exhibits relatively lower echolocation frequencies relative to body size compared with other rhinolophids, implying distinct evolutionary trajectories. Transcriptomes bridge genotypes and phenotypes. Here, we sequenced brain, liver and cochlea transcriptomes from one individual per species representing five taxa of the group. We performed comparative transcriptomic analyses and detected signals of positive selection. Seven hearing-related genes (, , , , , and ) were under positive selection. Unexpectedly, we also identified five vision-associated positively selected genes (, , , and ) in taxa with relatively lower echolocation frequencies within the group, indicating selection on sensory genes. Furthermore, candidate positively selected genes were significantly enriched in metabolism-related GO terms such as catalytic and oxidoreductase activity. Our study offers valuable transcriptomic resources for unraveling adaptive genetic mechanisms in horseshoe bats. - Source: PubMed
Publication date: 2026/07/30
Zhang LinSun KepingDai WentaoLiu TongLi AoqiangFeng Jiang - Spinal cord injury (SCI) triggers an immediate and sustained disruption of the composition and organization of the neuronal cytoskeleton. Radical alterations in axonal and dendritic microtubules characterize both the acute injury phase and the protracted recovery period. For decades, researchers have sought to correct these microtubule defects as a therapeutic strategy to encourage axonal regeneration, collateral sprouting, and the functional rewiring of neuronal circuits. Recent studies have demonstrated that taxol and related microtubule-active drugs improve outcomes in rodent models. These benefits are achieved by preventing microtubule depolymerization, stabilizing existing polymers, and promoting new assembly within both afflicted neurons and the glial cells essential for repair. While these findings highlight the therapeutic potential of microtubule-based interventions, we posit that successful clinical translation necessitates a more sophisticated approach rooted in the growing knowledge of microtubule-related proteins and their intricate regulatory mechanisms. This review evaluates progress in this arena, specifically examining the microtubule interactome network that includes structural microtubule-associated proteins (MAPs) such as Tau, MAP1A, MAP1B, MAP2, and MAP6, as well as the stathmin family, plus-end tracking proteins, and microtubule-severing proteins such as fidgetin and spastin. In addition, we analyze the contribution of molecular motor proteins and regulatory MAPs, including CRMP2 and CRMP4, as well as upstream transcription factors governing their expression. Finally, we address convergent regulation through kinases such as GSK3β and CDK5, which represent a central mechanistic axis linking injury signaling to cytoskeletal failure. By integrating data from studies on development and regeneration into a unified mechanistic model, we provide a framework for microtubule-based therapeutics for SCI. - Source: PubMed
Fischer ItzhakBaas Peter W - In frontotemporal dementia (FTD), tau detaches from axonal microtubules and forms pathological aggregates. Rather than stabilizing microtubules, tau promotes labile microtubule domains, redefining its role in neurodegeneration and underscoring the need for human models that capture temporal disease progression. - Source: PubMed
Sun XiaohuanRamakrishnan SkandhaOgbolu Victor CKanaan Nicholas MKarch Celeste MBaas Peter WQiang Liang - Kv3.3 voltage-gated K (Kv) channels are highly expressed in cerebellar Purkinje neurons and some hippocampal neurons, aligning with the motor and cognitive impairments observed in spinocerebellar ataxia 13 (SCA13) caused by Kv3.3 mutations. Despite their functional significance, the mechanisms governing Kv3.3 subcellular localization remain poorly understood. Here we report microtubule-associated protein 6 (MAP6) regulates Kv3.3 axon-dendrite targeting. MAP6 deletion reduces Kv3.3 levels in the processes of Purkinje neurons. Mechanistically, MAP6's 1st and 2nd Mn modules directly bind the external surface of the Kv3.3 N-terminal T1 tetramer, while its 3rd Mn module indirectly associates with Cav2 Ca channels. In Purkinje neurons, shRNA-mediated MAP6 knockdown decreases somatodendritic levels of both Kv3.3 and Cav2.1 (associated with SCA6). Notably, expression of Mn1/2-GFP selectively reduces Kv3.3, but not Cav2.1, levels. Purkinje neuron burst firing is reduced in both conditions. These findings uncover a MAP6-dependent mechanism for targeting two key ion channels linked to SCAs. - Source: PubMed
Publication date: 2026/04/30
Ma DiNalinakshan NandithaMarshall Alec HJukkola PeterBosc ChristopheGory-Fauré SylvieAndrieux AnnieWester Jason CGu Chen - Microtubule-associated Protein 6 (MAP6) is critical for maintaining microtubule stability and synaptic plasticity, and its dysfunction is a key driver of cognitive impairment. However, the molecular mechanisms linking MAP6 deletion to cognitive deficits remain unclear. Here, we generated a novel Map6 knockout (KO, Map6) mouse model using CRISPR/Cas9-mediated genome editing. Behavioral tests confirmed that Map6 mice exhibited prominent cognitive impairments, primarily in long-term memory and spatial learning. Hippocampal transcriptome profiling identified marked downregulation of neurotensin (Nts) in Map6 mice, which was validated at both mRNA and protein levels. Rescue experiments demonstrated that direct microinjection of neurotensin (NTS) peptide into the hippocampal CA1 subregion significantly improved cognitive deficits in Map6 mice. Electrophysiological recordings further confirmed that NTS restored impaired long-term potentiation (LTP)-a cellular substrate of learning and memory-in the hippocampal CA1 of Map6 mice. Additionally, chemogenetic activation of CA1 NTS-positive (CA1) neurons reversed these synaptic and behavioral phenotypes. Collectively, we delineate a novel pathway wherein MAP6 deletion induces cognitive impairment by suppressing hippocampal NTS expression and secretion, and both exogenous NTS supplementation and NTS signaling activation reverse Map6 deletion-induced synaptic and behavioral deficits. These findings identify NTS as a critical downstream effector of MAP6 in cognitive regulation, offering a potential therapeutic target for cognitive impairment. - Source: PubMed
Publication date: 2026/03/11
Jia YananLei JintaoJiang YunruiXue LitingChen TiantianWang JiaojiaoWei Hongen