Ask about this productRelated genes to: MAPK13 Blocking Peptide
- Gene:
- MAPK13 NIH gene
- Name:
- mitogen-activated protein kinase 13
- Previous symbol:
- PRKM13
- Synonyms:
- SAPK4, p38delta
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-28
- Date modifiied:
- 2016-10-05
Related products to: MAPK13 Blocking Peptide
Related articles to: MAPK13 Blocking Peptide
- Hybridization is a powerful evolutionary force for genetic improvement, conferring growth advantages and enhanced disease resistance. However, molecular basis of heterosis, especially when mediated by brain-derived neural regulation, remains unclear. To elucidate this, comparative brain transcriptome analysis was performed on red crucian carp, white crucian carp, their hybrid WR, and the backcross-improved WR-II. Our results revealed significant transcriptional changes between parents and their hybrids, leading to the identification of widespread differentially expressed genes (DEGs). Hierarchical clustering and quantitative mid-parent value analysis of DEGs revealed additive expression patterns in WR, whereas WR-II exhibited maternal bias in expression patterns. These DEGs were significantly enriched in pathways related to immune response, neural development, synaptic signaling, and insulin regulation. Weighted gene co-expression network analysis identified eight modules; one module significantly correlated with WR-II (r > 0.5, p < 0.01) contained the highest number of hub genes, totaling 71 (absolute kME value > 0.9). Protein-protein interaction network further highlighted key hub genes in WR-II, including NeuroD1, Rims2, KCND3, Gpc3, and MAPK13, exhibiting above the higher parent expression compared to parents. The encoded proteins form integrated networks central to insulin synthesis and secretion, neuronal excitability, growth regulation, and immune modulation. These findings provide new insights into neural mechanisms that contribute to heterosis in fish. - Source: PubMed
Publication date: 2026/05/26
Li RuZhang JipengWang JunZhou YiWang ChenghuiLiu Dong - This study focused on the synthesis of a novel series of (4-bromothiophen-2-yl)methyl 1-naphthoate derivatives (5a-5h) the Suzuki-Miyaura cross-coupling with moderate to excellent yields. Acute pentylenetetrazol (PTZ) and 6 Hz psychomotor seizure models were used to investigate anticonvulsant effects. The 5b, 5d, and 5h showed significant outcomes concerning mortality, protection, and seizure severity. In addition, the goal of the current study was to use a multifaceted strategy that integrates molecular docking (AutoDock Vina), ADMET (SwissADME, Molsoft), and network pharmacology to explore their potential as anti-epileptic drugs against important targets (GABAA receptor (8G5G), SV2A (3O7P, 1PW4)). To find common targets, we built PPI networks and carried out functional enrichment analysis. As compared to standard medications (levetiracetam, diazepam, and PTZ), all compounds (5a-5h) showed greater binding affinities (-7.6 to -9.7 kcal mol). ADMET profiles revealed drug-like characteristics with good bioavailability scores (0.55), but they also highlighted P-gp substrate liabilities and low solubility as important improvement considerations. Molsoft web server highlighted their good BBB permeation. By focusing on hub genes (SRC, AKT1, MAPK1/3, STAT3, EGFR) implicated in key signaling pathways such as PI3K-Akt, MAPK, JAK-STAT, and GABAergic synapse signaling, network analysis showed that these drugs had 15-25 targets in common with epilepsy. - Source: PubMed
Publication date: 2026/05/21
Mohsin NayabRasool NasirKanwal AqsaSaghir Khaled AhmedImran ImranSiddique FarhanNadeem SumairaImran Muhammad - Ovarian cancer (OC) is a highly aggressive malignancy with poor prognosis and limited response to immunotherapy. Ribosomal stress, a cellular response to disrupted ribosome biogenesis, has been increasingly implicated in tumorigenesis and immune regulation, yet its contribution to OC remains unclear. - Source: PubMed
Publication date: 2026/05/11
Han XuechuanYu YanFan YangZhang Miao - Skeletal muscle development directly determines growth efficiency and meat quality in livestock. Circular RNAs (circRNAs) and their encoded micropeptides are emerging regulators of this process, yet their roles in goats remain poorly understood. Through integrated ribosome profiling (Ribo-seq) and circRNA-seq of goat skeletal muscle satellite cells (SMSCs), we identified a MAPK1-derived protein-coding circRNA, circMAPK1 (novel-circ-0039015). Functional analyses revealed that circMAPK1 overexpression suppressed SMSCs proliferation and myogenic differentiation. Mechanistically, circMAPK1 encodes a 110-amino-acid micropeptide (circMAPK1-110aa) that binds Mitogen-Activated Protein Kinase Kinase 1 (MAP2K1) and reduces MAPK1/3 phosphorylation, thereby attenuating Mitogen-Activated Protein Kinase (MAPK) signaling. Importantly, pharmacological activation of the MAPK pathway with C16-PAF partially restored muscle cell growth and differentiation. These findings establish circMAPK1 as a negative regulator of goat skeletal muscle development and highlight its encoded micropeptides as a potential molecular target. By uncovering a new regulatory mechanism of muscle growth, this study provides valuable insights for breeding strategies aimed at enhancing meat yield and quality in goats. - Source: PubMed
Publication date: 2026/04/27
Pan QianqianLou MengyuZhu MengkangHe XiaohongLan XianyongZhang SihuanLing Yinghui - Fusobacterium nucleatum, a periodontal pathogen, has been increasingly implicated in pulmonary diseases including chronic obstructive pulmonary disease (COPD). This study demonstrates that F. nucleatum adheres to and invades pulmonary epithelial cells in a dose-dependent manner, primarily mediated by its adhesin FadA. We identify cadherin-11 (CDH11), which is upregulated in COPD lungs and in pulmonary epithelial cells treated with F. nucleatum or FadAc protein, as the key host receptor for FadA. This FadA-CDH11 interaction not only mediates bacterial adhesion and invasion, but also activates the MAPK13/JUN pathway, leading to significant upregulation of pro-inflammatory cytokines including CSF3, TNF-α, CCL20, and TGF-β. Genetic knockdown of CDH11 abolishes MAPK13/JUN activation and cytokine induction but does not affect FadA-mediated p53 suppression, indicating a separate pathway for this oncogenic event. Our findings establish the FadA-CDH11-MAPK13/JUN axis as a central mechanism driving F. nucleatum-exacerbated pulmonary inflammation and tissue damage, highlighting its potential as a therapeutic target for mitigating COPD progression. - Source: PubMed
Publication date: 2026/04/20
Liu KunXie XinyunLi YuchaoZhang ShuweiZang WenliLi QianPan Yaping