Tyrosine Kinase Adaptors Phospho-Specific Array includes 98 highly specific and well-characterized phosphorylation antibodies related to Tyrosine Kinase Adaptors.
- Known as:
- Tyrosine Kinase Adaptors Phospho-Specific Array includes 98 very specific well-characterized phosphorylation antibodies related Tyrosine Kinase Adaptors.
- Catalog number:
- AA0042
- Product Quantity:
- 2 Pieces/Box
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Tyrosine Kinase Adaptors Phospho-Specific Array includes 98 highly specific and well-characterized phosphorylation antibodies related Adaptors.
Related genes to: Tyrosine Kinase Adaptors Phospho-Specific Array includes 98 highly specific and well-characterized phosphorylation antibodies related to Tyrosine Kinase Adaptors.
- Gene:
- MAPK4 NIH gene
- Name:
- mitogen-activated protein kinase 4
- Previous symbol:
- PRKM4
- Synonyms:
- Erk3-related, Erk4
- Chromosome:
- 18q21.1-q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2018-02-13
Related products to: Tyrosine Kinase Adaptors Phospho-Specific Array includes 98 highly specific and well-characterized phosphorylation antibodies related to Tyrosine Kinase Adaptors.
Related articles to: Tyrosine Kinase Adaptors Phospho-Specific Array includes 98 highly specific and well-characterized phosphorylation antibodies related to Tyrosine Kinase Adaptors.
- Wheat germ glycoprotein (WGPII) exhibits immunomodulatory activity; however, its protective mechanisms against intestinal injury remain unclear. This study investigated WGPII effects in cyclophosphamide (CTX)-induced intestinal injury mice. WGPII significantly reversed immunosuppression by increasing serum cytokines and immunoglobulins and mitigated intestinal damage by upregulating SIgA and tight junction proteins. 16S rDNA sequencing and metabolomics revealed that WGPII enriched beneficial taxa (Lachnospiraceae_NK4A136_group, Roseburia) and decreased Bacteroides, correlating with TCA cycle activation and key metabolite enrichment (α-ketoglutarate, pyruvate, and N-acetyl-l-glutamate). WGPII also upregulated colonic miR-217-5p, miR-769-x, and miR-654-3p, while suppressing their predicted targets (Cxcl12, Mapk4, IL-17F). Correlation analysis suggested a potential "miRNA-gut microbiota-metabolite" regulatory network that may contribute to WGPII's protective effects. These correlational findings provide a theoretical basis for developing WGPII-based functional products for intestinal health, though direct mechanistic validation is warranted. - Source: PubMed
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Publication date: 2026/07/15
Jia MengYu Shi-LiSun Ping-Li - Alzheimer's disease (AD) is characterized by neuroinflammation, yet the impact of concurrent systemic infections on the AD brain remains poorly understood. We investigated the molecular mechanisms underlying the central nervous system response to systemic infections in AD by analyzing RNA sequencing data generated in the prefrontal cortex from 202 post-mortem donors (113 AD, 89 controls), where we stratified by the presence of a respiratory infection at the time of death. We identified 763 significant differentially expressed genes (DEGs) between AD and controls without infection, which were enriched for oxidative phosphorylation and neurodegenerative pathways. In contrast, 122 DEGs distinguished AD from controls during infection, with 57 genes uniquely altered in AD in the presence of infection, including MAPK4, VAV3, and POU3F4, implicating infection-dependent mechanisms of vascular and immune regulation. Pathway activity analysis revealed that infection in AD suppresses some immune and vascular pathways, while enhancing transcriptional and developmental programs. Weighted gene co-expression network analysis uncovered three key modules: one module strongly associated with AD, enriched for aging and signal transduction; one module linked to both AD and infection, highlighting cytoskeletal remodeling and host-pathogen interactions; and one module specific to infection, enriched in astrocytes, pericytes, and endothelial cells, implicating blood-brain barrier dysfunction. These findings suggest that systemic respiratory infections reshape transcriptional programs in the AD brain, dampening immune effector pathways and engaging vascular and host-pathogen processes in blood-brain-barrier-associated cell types. Our results highlight the complex interplay between systemic infection, neuroinflammation, and vascular responses in AD. - Source: PubMed
Publication date: 2026/06/26
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Publication date: 2026/06/25
Panagopoulos IoannisStranger AneSveen AnitaJareid MieKidd Susanne GBischof KatharinaTaskén KjetilDørum AnneDavidson BenLothe Ragnhild ASkotheim Rolf IJohannessen Bjarne - Canine flank alopecia (CFA) is a recurrent, seasonal, non-inflammatory skin disorder of uncertain etiology that affects several breeds, including Rhodesian ridgebacks. While endocrine and environmental influences have been suggested, the genetic background remains unclear. This study aimed to identify candidate genes associated with CFA in Rhodesian ridgebacks using a genome-wide approach. Low-pass whole-genome sequencing with imputation was performed on 48 Rhodesian ridgebacks (24 cases, 24 controls), followed by genome-wide association analyses and evaluation of protein-coding variants. Filtering for variants with predicted functional impact revealed variants in , EPB41L1, and DPY19L1, which are involved in cytoskeletal function, cell adhesion, neural signaling, and pathways critical for hair follicle cycling, such as Wnt, BMP, MAPK, Notch, and Hedgehog signaling. Our findings demonstrate that CFA is likely a skin disorder with genetic heterogeneity, where multiple loci and possibly modifier variants influence disease susceptibility, rather than a simple monogenic disorder. These results align with the complex inheritance observed in atypical recurrent flank alopecia, supporting a complex multifactorial etiology involving both genetic and environmental factors. This study provides the first insights into the genetic background of CFA in Rhodesian ridgebacks and highlights candidate genes for further functional investigation. Broader genomic approaches are needed to elucidate the disorder's genetic basis, ultimately guiding CFA-preventative breeding strategies. - Source: PubMed
Publication date: 2026/04/21
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