MAP2_RAT Map2 ELISA tesk kit
- Known as:
- MAP2_RAT Map2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17104
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- MAP2_RAT Map2 ELISA tesk kit
Related genes to: MAP2_RAT Map2 ELISA tesk kit
- Gene:
- MAP2 NIH gene
- Name:
- microtubule associated protein 2
- Previous symbol:
- -
- Synonyms:
- MAP2A, MAP2B, MAP2C
- Chromosome:
- 2q34
- Locus Type:
- gene with protein product
- Date approved:
- 1989-01-16
- Date modifiied:
- 2016-10-05
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- To evaluate time-dependent changes in retinal ganglion cell (RGC) dendrites and soma, as well as other retinal structural alterations, in a monkey ocular hypertension (OHT) model for preclinical glaucoma research. - Source: PubMed
Publication date: 2026/05/23
Yoshida SatoyoKishi Naoki - Alzheimer's disease (AD) is a neurodegenerative disorder that is caused by multiple factors, characterized by a progressive decline in cognitive ability, extracellular amyloid-β (Aβ) plaques, and intracellular neurofibrillary tangles composed of hyperphosphorylated tau. Current treatment strategies can provide only symptomatic treatment or limited efficacy, highlighting the need to intervene in the upstream regulatory factors that drive both amyloid and tau pathologies. Death-associated protein kinase 1 (DAPK1) is a key driver upstream of both amyloid precursor protein processing and tau phosphorylation, simultaneously promoting amyloidogenesis and tau-mediated pathology in AD. In this study, we developed CP1, a bifunctional proteolysis-targeting chimera (PROTAC), to recruit E3 ubiquitin ligase to DAPK1, thereby inducing the ubiquitination and proteasomal degradation of DAPK1. CP1 efficiently eliminated the DAPK1 protein in primary cortical neurons without affecting its mRNA level, resulting in reduced Aβ generation and tau hyperphosphorylation. , upon systemic administration, CP1 effectively crossed the blood-brain barrier, degraded DAPK1, and consequently reduced the Aβ plaque burden and mitigated neuroinflammation in female 5xFAD mice. In a AAV-hTau-P301L tauopathy model, CP1 treatment suppressed tau hyperphosphorylation, preserved NeuN- and MAP2-positive neurons, attenuated astrocytic and microglial activation, and ultimately restored learning and memory abilities in both male and female mice. In summary, these findings demonstrate that degrading DAPK1 via a PROTAC strategy simultaneously mitigates both amyloid and tau pathology, indicating that CP1 is an effective candidate for disease-modifying therapy. - Source: PubMed
Publication date: 2026/04/23
Li RuomengYao JingPeng WenZheng LizhenWu XueyinShui XindongZheng XiaoqingTian WujinWang LongZhou YingRuan XinglinPan XiaodongZhang TaoLiu YangLee Tae HoChen Dongmei - Intracerebral hemorrhage (ICH) is a neurological disorder characterized by a high mortality rate for which there is currently no definitive cure. Research has demonstrated that adipose-derived mesenchymal stem cells (ASCs) exhibit considerable potential in treating ICH. However, the advanced age of ICH patients and the necessary cell expansion before transplantation therapy could result in the senescence of ASCs, thereby compromising their viability and therapeutic efficacy. This study aims to investigate whether FGF21 (fibroblast growth factor 21) can rejuvenate aged ASCs by enhancing macroautophagy/autophagy flux and subsequently enhance the therapeutic efficacy of ICH. We demonstrated that the autophagy flux of aged ASCs was significantly decreased and FGF21 treatment significantly reversed the senescence phenotype and increased the viability of aged ASCs. Mechanistically, our findings suggested that FGF21 rejuvenates aged ASCs by augmenting autophagy flux, a process partly mediated by TFE3 (transcription factor E3) nuclear translocation. The FGF21-induced TFE3 nuclear translocation was partially facilitated potentially via the FGFR1-SIRT1-MTOR pathway. In addition, FGF21 enhanced the potential of senescent ASCs to differentiate into neurons. In the in vivo study, we further verified that FGF21 could enhance the therapeutic effect of ASCs on acute ICH rats. In conclusion, these results indicated that FGF21 could restore ASC viability by upregulating TFE3-mediated autophagy flux in part through the FGFR1-SIRT1-MTOR signaling pathway, enhanced the potential to improve the differentiation of ASCs into neural stem cells and enhanced the therapeutic effect of ASCs transplantation in acute ICH.: FGF21: fibroblast growth factor 21; TFE3: transcription factor E3; TFEB: transcription factor EB; DMEM: Dulbecco's modified Eagle medium; RAPA: rapamycin; 3-MA: 3-methyladenine; CQ: chloroquine; DMSO: dimethyl sulfoxide; RT-qPCR: quantitative real-time PCR; pAb: polyclonal antibody; mAb: monoclonal antibody; LAMP1: lysosomal associated membrane protein 1; SQSTM1/p62: sequestosome 1; MAP1lc3/LC3: microtubule associated protein 1 light chain 3; GFAP: glial fibrillary acidic protein; MAP2: microtubule associated protein 2; SOX2: SRY-box transcription factor 2; MOI: multiplicity of infection; FGFR1: fibroblast growth factor receptor 1; SIRT1: sirtuin 1; MTOR: mechanistic target of rapamycin kinase; ROS: reactive oxygen species; siRNA: small interfering RNA; OD: optical density; SASP: senescence-related secretion phenotype; IL6: interleukin 6; IL1B/IL-1β: interleukin 1 beta; TNF/TNF-α: tumor necrosis factor; CCL2/MCP-1: C-C motif chemokine ligand 2; BDNF: brain derived neurotrophic factor; VEGF: vascular endothelial growth factor; ICH: intracerebral hemorrhage; MLPT: modified limb placement test. - Source: PubMed
Publication date: 2026/05/19
Song BeiLiu ChengyunHu JingqiongZhao XiaofangFan HaohuiLiu TingGao GuangyuZhang XinyueGuang XuekeZhou QuanWang KunLu Weilin - Type 2 diabetes has been associated with cognitive decline and an increased risk of neurodegenerative diseases, although the cellular mechanisms underlying this relationship remain unclear. We investigated whether high-glucose exposure induces neuronal damage and increases susceptibility to secondary oxidative and neurotoxic insults in vitro. SH-SY5Y cells were differentiated into neuron-like cells and exposed to increasing glucose concentrations. Based on the viability results, cells exposed to high glucose (HG; 100 mM, 120 h) were further analyzed and challenged with hydrogen peroxide (HO) or okadaic acid (OA). Cell viability, DNA damage, mitochondrial superoxide production, cell cycle distribution, cell death, and gene expression were evaluated. Differentiation was confirmed by increased neurite length and expression of neuronal markers (β-III-tubulin and MAP2). High glucose reduced cell viability in a concentration- and time-dependent manner. HG exposure increased oxidative DNA damage, mitochondrial superoxide levels, and apoptosis, accompanied by reduced OGG1 gene expression. Combined treatments with HG and HO or OA further decreased cell viability and increased the sub-G1 fraction compared with controls and single treatments. These findings demonstrate that HG exerts cytotoxic and genotoxic effects and sensitizes neuron-like cells to subsequent oxidative and neurotoxic insults, thereby contributing to mechanisms underlying neuronal dysfunction and neurodegenerative processes. - Source: PubMed
Publication date: 2026/05/19
Lima Jéssica Ellen Barbosa de FreitasMoreira Natália Chermont Dos SantosPiassi Larissa de OliveiraOno Renata Melo Dos SantosSakamoto-Hojo Elza Tiemi - Alpha-Lipoic Acid (ALA) is known for its antioxidant and antiinflammatory properties; however, its direct role in neurogenesis remains undefined. This study evaluated the neurogenic potential of the R-enantiomer (R-ALA) using transcriptomic profiling and in vitro validation. - Source: PubMed
Publication date: 2026/05/11
Gupta SamriddhiKaushal ShrutiBhargava PriyanshuIshida YoshiyukiTerao KeijiKaul Sunil CDhanjal Jaspreet KaurWadhwa Renu