Ask about this productRelated genes to: MAP2B antibody
- 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
Related products to: MAP2B antibody
Related articles to: MAP2B antibody
- Understanding the pathogenesis of paratuberculosis (PTB), caused by Mycobacterium avium subspecies paratuberculosis (MAP), is essential in the management of this economically important disease. MAP strains are known to differ genotypically, which could contribute to differences in strain virulence and disease outcomes. The behaviour of MAP inside the host and the mechanisms utilized by MAP to overcome the host defence system are not entirely understood. This study aimed at evaluating the potential virulence of different MAP isolates from cattle in Uganda. This was achieved by analysing the cytokine expression profiles of RAW 264.7 macrophages when infected with four different MAP isolates: MAP1, MAP2, MAP3 and MAP4. Specific real-time PCR was used to determine the expression of different cytokines, probable virulence genes of MAP as well as MAP quantities inside the macrophages at different time points (3 h, 24 h, 48 h) post-infection (pi). There were considerable variations in the cytokine expressions among macrophages infected with the different MAP isolates. The expression of IL-6 in macrophages infected with MAP1 at 48 h pi was noticeably high compared to the other isolates; and this is a known strategy for MAP survival inside macrophages. The regulation of the probable virulence genes: kdpC, katG, papA2, impA, umaA1, and the anti-apoptotic (BCL-2) gene also varied considerably among the isolates. Isolates MAP1, MAP2 and MAP3 demonstrated higher virulent behaviour regarding intracellular replication and survival compared to MAP4 isolate. The behaviour of these MAP isolates clearly indicates variations in virulence and further research needs to focus on how this can be exploited in the design of PTB diagnostic and control strategies. - Source: PubMed
Publication date: 2026/05/06
Ssekitoleko JudahTanneberger FranziskaEltom Kamal HEltayeb ElSagadTruyen UweOjok LonzyAmanzada AhmadWampande EdwardNsubuga Moses LuutuSebulime PeregrineAbd El Wahed AhmedOkuni Julius Boniface - Mitogen-activated protein kinase kinase 4 (MKK4), a MAP2 kinase that activates c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase, is a key kinase of the stress-activated protein kinase (SAPK)/mitogen-activated protein kinase (MAPK) signaling network. Inhibition of MKK4 represents a novel therapeutic approach by leveraging a rerouting mechanism within the signaling network, predominantly via MKK7 and JNK1, to modulate the regenerative capacity of hepatocytes. In this study, we describe the discovery of darizmetinib (HRX215), a first-in-class MKK4 inhibitor currently in clinical development. Darizmetinib was derived from a known BRaf inhibitor, and through extensive structure-activity relationship (SAR) studies, we successfully engineered potency and selectivity for MKK4 while eliminating the original BRaf on-target activity. Preclinical proof-of-concept studies, along with evaluations of different lead candidates, identified darizmetinib, demonstrating dose-dependent efficacy across various disease-relevant pharmacological models. - Source: PubMed
Publication date: 2026/05/06
Albrecht WolfgangSelig RolandPfaffenrot BentKloevekorn PhilipJuchum MichaelZwirner StefanKlotz SabrinaZender LarsLaufer Stefan - Schizophrenia is a complex neurodevelopmental disorder with cognitive impairment being one of the core features that remains largely unresponsive to current antipsychotic treatments. Histone deacetylase 3 (HDAC3), a negative regulator of memory and synaptic plasticity, has been implicated in neurodegenerative conditions, but its role remains underexplored in psychosis. Here, we hypothesized that aberrant HDAC3 activity contributes to hippocampal dysfunction and learning deficits in schizophrenia. Pregnant SD rats were administered methylazoxymethanol (MAM; 20 mg/kg) and vehicle on GD 17. We characterized the pharmacokinetic profile of selective HDAC3 inhibitor, SP108, to ensure adequate BBB penetration and systemic exposure. Next, adult male offspring were administered SP108 (25 mg/kg, i.p.) and vehicle every day for 3 weeks, followed by behavioral analysis. The MAM-exposed group showed schizophrenia-like behavioral patterns with increased hippocampal HDAC3 expression and activity. HDAC3 inhibitor treatment selectively ameliorated avoidance learning and MK801-induced hyperlocomotion. At the molecular level, HDAC3 inhibition elevated hippocampal H3K9 acetylation and increased the expression of synaptic plasticity markers BDNF and PSD95. To establish a neurodevelopmental link, HDAC3 knockdown was performed in differentiating neurons from mouse embryonic stem cells (mESCs) exposed to MAM at the early differentiating phase in vitro. HDAC3 knockdown in MAM-exposed differentiating neurons enhanced MAP2 intensity and neurite length with improved levels of MAP2, NeuN, TUBB3 (neuronal differentiation and maturation markers), BDNF, and PSD95 (neuroplasticity markers). Collectively, these findings identify HDAC3 as an important regulator of hippocampal dysfunction and cognitive impairment in a schizophrenia-like preclinical model, highlighting its potential to augment the therapeutic outcomes beyond current antipsychotic treatments. - Source: PubMed
Publication date: 2026/04/30
Ghosh AparajitaAmbati HimajaRegula SanjeevTashildar MuktaKalita AbhipshitGanorkar AbhiramAnne AnuhyaMohan Kommu NagaKulkarni Onkar PrakashGhosh Balaram - Spinal cord injury (SCI) induces a detrimental secondary inflammatory cascade driven largely by pro-inflammatory M1 macrophages, which impedes neural repair. Tetramethylpyrazine (TMP), a bioactive alkaloid from Ligusticum chuanxiong, has shown promise in modulating neuroinflammation. In this study, Sprague-Dawley rats subjected to thoracic contusion SCI received daily intraperitoneal TMP at 60 mg/kg or 80 mg/kg for 7 days. TMP treatment significantly improved hindlimb motor function, as evidenced by higher Basso-Beattie-Bresnahan (BBB) locomotor scores from day 7 through day 28 post-injury and increased motor evoked potential (MEP) amplitudes at day 28, confirming enhanced motor pathway conduction. Histological analyses (HE and Nissl staining) revealed reductions in lesion cavitation, preservation of neuronal architecture, and attenuated glial scar formation in TMP-treated groups. Immunofluorescence demonstrated increased NeuN, MAP2, and NF200 and decreased GFAP expression, while double staining for iNOS/CCR2 and Arg1/CCR2 indicated a shift from M1 to M2 macrophage polarization. ELISA showed significant reductions in IL-6 and TNF-α and elevation of IL-10, and both WB and RT-qPCR confirmed TMP-mediated suppression of IL-6/JAK2/STAT3 phosphorylation and gene transcription. In vitro, TMP reversed LPS-induced M1/M2 polarization imbalance in RAW 264.7 cells, meanwhile suppressing IL-6/JAK2/STAT3 phosphorylation and gene transcription, reduced pro-inflammatory cytokine release in TMP groups. Furthermore, rescue experiments demonstrated that co-treatment with recombinant IL-6 reversed TMP-mediated suppression of JAK2/STAT3 phosphorylation and M1-to-M2 polarization shift, confirming the IL-6/JAK2/STAT3 pathway as a direct mechanistic target of TMP. These results indicate that TMP fosters histopathological and functional recovery after SCI by reshaping macrophage polarization via inhibition of the IL-6/JAK2/STAT3 pathway, highlighting its potential as an anti-inflammatory neuroprotective therapy. - Source: PubMed
Publication date: 2026/04/30
Bai HuizhongHuo LuyaoYu RuiqinDeng BowenYue JiashuJiang YuZhou YiminZhao YiMu Xiaohong - Substance use disorders (SUDs) are highly associated with other mental health conditions and disparities exist across sociodemographic characteristics. We aimed to estimate the incidence of specific SUDs and comorbidities with United States electronic health record data. - Source: PubMed
Publication date: 2026/04/23
Parker Maria AAhmedani Brian KYeh Hsueh-Han