MAPK13 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- MAPK13 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100065
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MAPK13 antibody Polyclonal Antibodies Primary antibodies
Related genes to: MAPK13 antibody Polyclonal Antibodies Primary antibodies
- 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 antibody Polyclonal Antibodies Primary antibodies
Related articles to: MAPK13 antibody Polyclonal Antibodies Primary antibodies
- Airborne particulate matter 10 (PM10) induces lung inflammation. However, interventions remain limited. We evaluated the protective effects of Chrysanthemum zawadskii var. latilobum (CZL) against PM10-induced lung injury using an integrated strategy combining phytochemical profiling, network pharmacology, deep-learning molecular docking, and in vivo/in vitro validation. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) profiling identified 52 phytochemicals in the 50% ethanol CZL extract. The network pharmacology analyses converged on the PI3K-AKT and mitogen-activated protein kinase (MAPK) signaling pathways. Molecular docking predicted strong binding affinities (ΔG ≤ -7 kcal/mol) for flavonoids such as luteolin, quercetin, apigenin, and eupatilin toward PIK3CA, AKT1, and MAPK1/3. Our PM10-induced lung inflammation model systems validated that CZL reduced PM10-induced phosphorylation of AKT and ERK, thereby dampening downstream cytokine expression, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Collectively, CZL exerts anti-inflammatory effects in pollution-related lung injury and suggest its potential as a functional food candidate for improving respiratory health. - Source: PubMed
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Jo Hyun SunHwang JinheeKim Min JaeJeong Jong HwiChoi Jae MunHong Ji YounKim Young JunHan Bok Kyung - Hepatocellular carcinoma (HCC), the third leading cause of cancer mortality, is targeted by Lenvatinib-a multi-receptor tyrosine kinase (RTK) inhibitor suppressing VEGFR/FGFR signaling. This study explored whether lenvatinib modulates the tumor metabolic microenvironment to inhibit HCC progression. - Source: PubMed
Publication date: 2026/04/14
Zhao XiaofangYan ShengxiangMeng JingWang Limin - Copy number variants (CNVs) are large-scale genomic alterations that contribute substantially to genetic diversity and may influence phenotypic variation in livestock. This study investigated the genome-wide CNV landscape of three Vietnamese indigenous chicken breeds. Whole-genome sequencing on the Illumina platform (3-5× coverage) was performed on 24 individuals from Dong Tao (DT), Cay Cum (CC), and Ri (RI) breeds. A total of 1743 CNVs were detected, clustering into 315 copy number variation regions (CNVRs). Most CNVRs were rare, with 31.7% present in only one animal among breeds. Across the genome, 122 unique CNVRs were distributed over 28 chromosomes, predominantly the first five. Losses were the most frequent type (45.9%), followed by gains (39.3%), and mixed events (14.8%). Within these CNVRs, 3633 genes were identified. In DT and RI, CNVR-embedded genes included several candidates, potentially related to adaptability, development, and phenotypic diversification. Notably, DT harbored genes such as , , , (adaptation, stress/immune response) and , , , , , , , and (developmental and skeletal traits), whereas in RI they included genes such as , , , and , which may contribute to muscle, bone, and physiological regulation. Functional enrichment analysis revealed numerous genes and Quantitative Trait Loci (QTLs) associated with metabolic, developmental, and immune-related pathways. This study provides the first comprehensive genome-wide CNV profile of Vietnamese indigenous chickens and offers a valuable genomic resource for investigating the genetic basis of breed-specific and adaptive phenotypes. - Source: PubMed
Publication date: 2026/04/01
Nguyen Thuy Thi-DieuTzvetkova AnaBui Mai Thi-DieuDo Vo-Anh-KhoaDinh Thuy Thi-NgocNguyen Phuong ThanhKuss Andreas WalterPenasa MauroCendron Filippo - Early pregnancy is a highly coordinated process requiring precise embryo-maternal communication. Estradiol-17β (E2) is considered the primary conceptus-derived signal responsible for the maternal recognition of pregnancy in pigs. Successful pregnancy establishment requires two distinct peaks of E2 secretion by porcine conceptuses: during days 11-12 (the maternal recognition of pregnancy) and days 15-30 (implantation). Although the role of E2 in signaling to the maternal system is well established, its potential autocrine effects on conceptus development remain unclear. This study examined whether E2 regulates trophoblast function during the maternal recognition of pregnancy and implantation. We demonstrated that expression of estrogen receptors (ESR1, ESR2, GPER1) and selected pregnancy-related genes (FOXO3, GDF15, SERPINE1, ESRRB, ESRRG) changes during early pregnancy in the pig. E2 regulated the gene expression of its receptors (ESR1, ESR2, GPER1), genes involved in E2 synthesis (HSD17B1), prostaglandin synthesis (PTGS2, AKR1C4, PTGES), and key mediators of pregnancy establishment (IL1B2, SERPINE1, FOXO3, GDF15, ESRRB and ESRRG). Furthermore, E2, acting via nuclear estrogen receptors, enhanced trophoblast cell proliferation on days 12 and 15 of pregnancy, and increased adhesion as well as MAPK1/3 and PTK2 protein phosphorylation on day 15 of pregnancy. E2 stimulated cell proliferation via MAPK and PI3K/AKT/mTOR pathways, whereas E2-promoted adhesion was mediated via MAPK and PI3K/AKT signaling. Concluding, these findings indicate that E2 functions not only as a critical embryonic signal for the maternal recognition of pregnancy but also plays an autocrine role in conceptus development, regulating gene expression and trophoblast cell function during early gestation in pigs. - Source: PubMed
Publication date: 2026/04/11
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Publication date: 2026/03/10
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