CCL22 Antibody (Center) Blocking Peptide
- Known as:
- CCL22 Antibody (Center) Blocking Peptide
- Catalog number:
- BP16351c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CCL22 Antibody (Center) Blocking Peptide
Related genes to: CCL22 Antibody (Center) Blocking Peptide
- Gene:
- CCL22 NIH gene
- Name:
- C-C motif chemokine ligand 22
- Previous symbol:
- SCYA22
- Synonyms:
- MDC, STCP-1, ABCD-1, DC/B-CK, A-152E5.1, MGC34554
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
Related products to: CCL22 Antibody (Center) Blocking Peptide
Related articles to: CCL22 Antibody (Center) Blocking Peptide
- 2,4-Di-tert-butylphenol (2,4-DTBP) is an emerging alkylphenol antioxidant with potential neurotoxicity concerns, but its molecular toxicological basis remains poorly defined. Here, we applied an integrated framework combining network toxicology, machine learning-assisted target prioritization, molecular docking, cellular validation, and integrated transcriptomic-metabolomic profiling to delineate 2,4-DTBP-induced neurotoxic mechanisms. Network toxicology implicated PI3K/AKT, MAPK, calcium signaling, cytokine-cytokine receptor interaction, and ATP-binding cassette (ABC) transporter pathways as major 2,4-DTBP-associated axes. By integrating three machine learning algorithms including least absolute shrinkage and selection operator (LASSO) regression, support vector machine-recursive feature elimination (SVM-RFE), and random forest (RF), we convergently prioritized six candidate genes potentially associated with 2,4-DTBP-related neurotoxicity: Erb-B2 receptor tyrosine kinase 2 (ERBB2), colony-stimulating factor 1 receptor (CSF1R), RET proto-oncogene (RET), C-C motif chemokine ligand 22 (CCL22), ATP-binding cassette subfamily C member 5 (ABCC5), and ATP-binding cassette subfamily C member 1 (ABCC1). SHapley Additive exPlanations (SHAP) quantified their contributions and improved model interpretability, while molecular docking provided preliminary structural insights into the potential interactions between 2,4-DTBP and its corresponding target proteins. In SH-SY5Y cells, 100 μM 2,4-DTBP exposure elicited pronounced cytotoxicity characterized by oxidative stress, mitochondrial alterations, lipid peroxidation, intracellular iron accumulation, apoptosis, ferroptosis-related perturbations, and pronounced inflammatory responses. Western blotting further confirmed alterations in the phosphorylation levels of AKT, ERK, NF-κB p65, and CaMKII. Ferrostatin-1 mitigated the 2,4-DTBP-induced reduction in cell viability, oxidative stress, mitochondrial dysfunction, lipid peroxidation, Fe accumulation, and cell death, while partially restoring the transcriptional changes in GPX4, SLC7A11, GCH1, and ACSL4. Multi-omics integration further revealed coordinated disruption of inflammatory programs, synapse-related pathways, amino acid and energy metabolism, and redox homeostasis. Collectively, these results support a multi-level mechanistic framework for understanding 2,4-DTBP-induced neurotoxicity and identify candidate molecular targets and potential biomarkers for assessing the environmental neurotoxicity risks of emerging phenolic contaminants. - Source: PubMed
Publication date: 2026/10/01
Zhu JinchaoLi JianxinLi WenjingLiu YanqingShi YueIbrahim NayabDong JinruiFan Haojun - c-MET overexpression is common in non-small cell lung cancer (NSCLC) and associated with poor prognosis, however, its role in immune evasion and immunotherapy resistance remains unclear. - Source: PubMed
Publication date: 2026/09/30
Chen LijinYao XihuSu ChunyangZheng JinyangFan RencaiZhang LipingChen HaoLi XiaofengLin Xiaoyan - The mechanism underlying myelofibrosis, which is associated with poor prognosis in myelodysplastic syndromes (MDS), remains unclear. - Source: PubMed
Maekawa TakaakiMukai NobuyukiYanaki YurikaKemmoku EmiShonai TakutoKawasaki KotaSone TakehiroTakada KoheiOgata HirakuSaito KeitaTachi NoriakiKawamura ToshikuniKato ShoichiroOsawa YukikoKobayashi Shinichi - Excessive inflammation is a critical contributor to impaired oral mucosal wound healing, yet effective therapeutic strategies are still lacking. Although dehydrocorydaline (DHC) has been reported to exhibit anti-inflammatory and analgesic properties, its role in wound healing and the underlying mechanisms have not been fully elucidated. This study aimed to investigate whether DHC accelerates palatal wound healing and to elucidate the role of the p38 mitogen-activated protein kinase (MAPK)/CCL2 signaling axis in DHC-mediated regulation of macrophage chemotaxis. , macrophages were stimulated with 1 μg/mL lipopolysaccharide (LPS) and treated with DHC at 0.1, 1, and 10 μM. The chemotactic response and inflammatory function of macrophages were assessed using real-time PCR, ELISA, Western blotting, and Transwell assays. Molecular docking simulations and Western blotting analyses were performed to examine the regulatory effect of DHC on MAPK signaling pathway. , a full-thickness palatal mucoperiosteal wound extending from the left maxillary first to third molars was established in mice by scalpel scraping. The effects of topical 10 μM DHC gel on wound healing were evaluated using stereomicroscopy, histological staining, and real-time PCR at 0, 3, and 5 days post-modeling. , DHC effectively downregulated the expression of chemokines, including C-C motif chemokine ligand 2 (), , , C-X-C motif chemokine ligand 10 (), and , with the most significant inhibitory effect on (70.8% inhibition). In Transwell assays, DHC reduced macrophage migration by 68.2%. Mechanistically, DHC prominently inhibited the activation of the MAPK signaling pathway. , DHC treatment accelerated wound healing and markedly reduced macrophage infiltration in mouse palatal wound tissues. These findings demonstrated that DHC accelerated palatal wound healing 1.6-fold in mice. DHC suppressed macrophage chemotaxis by 68.2% through modulation of the MAPK signaling pathway. - Source: PubMed
Publication date: 2026/08/27
Chen YingyiLiu ZhaonaWang YijiaXia GuiyangLiu YitongXia HuanWang MinfengLin ShengLiu Yi - Maternal inflammation is linked to adverse maternal and fetal outcomes, but how maternal inflammation affects fetal inflammation during mid-gestation is not known. - Source: PubMed
Goin Dana ELi LinGaw Stephanie LMorello-Frosch RachelWoodruff Tracey JEick Stephanie MRobinson Joshua F