MAPK3 & MAPK14 Protein Protein Interaction Antibody Pair
- Known as:
- MAPK3 & MAPK14 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0008
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MAPK3 & MAPK14 Protein Interaction Antibody Pair
Related genes to: MAPK3 & MAPK14 Protein Protein Interaction Antibody Pair
- Gene:
- MAPK3 NIH gene
- Name:
- mitogen-activated protein kinase 3
- Previous symbol:
- PRKM3
- Synonyms:
- ERK1, p44mapk, p44erk1
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2015-09-03
- Gene:
- MAPK14 NIH gene
- Name:
- mitogen-activated protein kinase 14
- Previous symbol:
- CSPB1, CSBP1, CSBP2
- Synonyms:
- PRKM14, p38, Mxi2, PRKM15
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-24
- Date modifiied:
- 2016-10-05
Related products to: MAPK3 & MAPK14 Protein Protein Interaction Antibody Pair
Related articles to: MAPK3 & MAPK14 Protein Protein Interaction Antibody Pair
- Non-alcoholic fatty liver disease (NAFLD) is a major global health concern with no specific approved pharmacological treatments. While (HS) shows therapeutic potential, its multi-target molecular mechanism remains unelucidated. This study pioneers a highly novel and integrated computational strategy combining network pharmacology, validated structure-based pharmacophore modeling, molecular docking, molecular dynamics simulations (MDs), and binding free energy calculations. Utilizing a unique and comprehensive compound library of HS phytochemicals, this rigorous methodology offers superior accuracy for mechanism elucidation. Network analysis revealed that HS primarily modulates the Lipid and Atherosclerosis pathway. A key novel finding was the identification of ten regulatory hub targets, including the critical components AKT1, MAPK1, MAPK3, CASP3, JAK2, MAPK14, EGFR, mTOR, IGF1, and IL6. By developing specific pharmacophore models for these targets, we stringently screened the compound library, successfully pinpointing four top-scoring phenolic constituents: P16 (blestrin A), P21 (dendrocandin I), P29 (octahydrocurcumin) and P32 (tribulusamide B). MDs confirmed these compounds possess superior binding affinities, predicting their function as potent multi-target agents against NAFLD. This work is the first to systematically propose the multi-target mechanism of HS, pinpointing these specific, high-affinity phytochemicals and their associated molecular hubs. These findings provide a robust molecular foundation, prioritizing these HS-derived compounds and targets for subsequent in vitro and in vivo experimental validation to accelerate the development of novel NAFLD therapeutics. - Source: PubMed
Publication date: 2026/02/26
Nguyen Chau Uyen PhuongLe Quynh Nguyen NhuNguyen Phuong Thuy VietNguyen Huong-Giang Thi - Imidacloprid is frequently detected as a residue in food commodities, raising concerns about potential human health risks. Previous findings remain fragmented, and no study has systematically elucidated the primary human target organs and underlying mechanisms using an integrative systems toxicology framework. We applied a human-specific network toxicology approach to characterize imidacloprid-induced toxicity comprehensively. By integrating target prediction and ADME/toxicity models (ADMETlab 3.0, admetSAR 3.0, and ProTox 3.0), the study identified three primary human-relevant toxicity endpoints (respiratory toxicity, liver injury, and genotoxicity/carcinogenicity). Protein-protein interaction, GO, and KEGG pathway analyses revealed that MAPK, NF-κB, JAK-STAT, UPR-ER stress, and Wnt signaling networks may be key pathways involved in oxidative stress, inflammatory signaling, cell-cycle dysregulation, and apoptosis. Molecular docking analysis further supported relatively stronger predicted binding of imidacloprid to several upstream regulatory proteins, including PTGS2 (COX-2), NOS3 (eNOS), APC, CDH1 (cadherin-1 or E-cadherin), AR, HSPA5 (GRP78 or BiP), HSP90AA1 (HSP90α), JAK2, and RELA (p65), whereas downstream signaling proteins such as MAPK14 (p38α), MAPK1 (ERK2), MAPK3 (ERK1), NFKB1 (p50/p105), WNT3A (Wnt), TNF (TNF-α), ESR1 (ERα), and BCL2 exhibited moderate predicted binding. Although these findings are derived from computational analyses and do not establish functional disruption, the coordinated involvement of upstream and downstream signaling hubs suggests possible mechanisms through which imidacloprid exposure may influence multiple organ systems. Taken together, this study provides a systems-level, hypothesis-generating framework to support future experimental validation and human health risk assessment. - Source: PubMed
Publication date: 2026/01/02
Boonyong CherdsakPowthong Pannapa - This study aimed to investigate the expression of cluster of differentiation 7 (CD7) in hepatoblastoma (HB) and its potential use as a novel biomarker of HB. - Source: PubMed
Publication date: 2025/12/04
Adawy AhmadYoshii DaikiHirao HirokiKomohara YoshihiroFujiwara YukioTomita MasahiroHonda MasakiHan JiaLiu YaoYamada SohsukeYamamoto MasahiroHiyama EisoHibi Taizo - Luminal B breast cancer (LBBC) is on the rise worldwide, with both incidence and mortality rates steadily increasing. Early detection proves difficult due to its aggressive characteristics, most notably its heightened proliferation rate and the complex interplay of molecular biomarkers, particularly in more advanced stages. - Source: PubMed
Publication date: 2025/08/15
Saeidi YousefGhorbani MasoudNajafi AliMoosazadeh Moghaddam Mehrdad - extract (LEE), rich in shikonin and its derivatives, has been traditionally valued for anti-inflammatory and wound-healing properties. - Source: PubMed
Publication date: 2025/09/29
Chi XiaoqingPing LiGai RenhuaWeng Qinjie