Dog Tissue Paraffin Sections Skin
- Known as:
- Dog Tissue Paraffin Sections Skin
- Catalog number:
- DP-101
- Product Quantity:
- 10 slides
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- Dog Tissue Paraffin Sections Skin
Related genes to: Dog Tissue Paraffin Sections Skin
- Gene:
- CCL27 NIH gene
- Name:
- C-C motif chemokine ligand 27
- Previous symbol:
- SCYA27
- Synonyms:
- ALP, ILC, CTACK, skinkine, ESkine, PESKY, CTAK
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: Dog Tissue Paraffin Sections Skin
(Ser140)-Myelin Proteolipid Protein (139-151) (depalmitoylated) (human, bovine, dog, mouse, rat)
(Ser140)-Lipophilin (139-151) (depalmitoylated) (human, bovine, dog, mouse, rat), (Ser140)-PLP (139-151(Ser140)-Myelin Proteolipid Protein (139-151) (depalmitoylated), human, bovine, dog, mouse, rat(Ser140)-Myelin Proteolipid Protein (139-151) (depalmitoylated), human, bovine, dog, mouse, rat(Ser140)-Myelin Proteolipid Protein (139-151) (depalmitoylated), human, bovine, dog, mouse, rat(Ser140)-Myelin Proteolipid Protein (139-151) (depalmitoylated), human, bovine, dog, mouse, rat(Ser140)_Myelin Proteolipid Protein (139_151) (depalmitoylated) (human, bovine, dog, mouse, rat) Salt Trifluoroacetate Binding _ Synonym (Ser140)_Lipophilin (139_151) (depalmitoylated) (human, bovi(Ser140)_Myelin Proteolipid Protein (139_151) (depalmitoylated) (human, bovine, dog, mouse, rat) Salt Trifluoroacetate Binding _ Synonym (Ser140)_Lipophilin (139_151) (depalmitoylated) (human, bovi(Ser140)_Myelin Proteolipid Protein (139_151) (depalmitoylated) (human, bovine, dog, mouse, rat) Salt Trifluoroacetate Binding _ Synonym (Ser140)_Lipophilin (139_151) (depalmitoylated) (human, bovi(Ser140)_Myelin Proteolipid Protein (139_151) (depalmitoylated) (human, bovine, dog, mouse, rat) Salt Trifluoroacetate Binding _ Synonym (Ser140)_Lipophilin (139_151) (depalmitoylated) (human, bovi(Ser140)_Myelin Proteolipid Protein (139_151) (depalmitoylated), human, bovine, dog, mouse, rat(Ser140)_Myelin Proteolipid Protein (139_151) (depalmitoylated), human, bovine, dog, mouse, rat(Tyr0)-C-Peptide (dog) 98% C146H234N38O51 CAS: 101135-67-5(Tyr0)_C_Peptide (dog) Salt _ Binding _ Synonym SumFormula C146H234N38O51(Tyr0)_C_Peptide (dog) Salt _ Binding _ Synonym SumFormula C146H234N38O51([125I]-Tyr)-BNP-34 (3-34) (dog) Related articles to: Dog Tissue Paraffin Sections Skin
- Psoriasis patients were 4- 5 times more likely to have S. aureus colonize their skin. Psoriasis is caused by staphylococcal infection-induced keratinocyte death, which is maintained by elevated cytokine production of TNF-α and IFN-γ. The study sought to determine the association between the influence of gene expression of certain genes in psoriasis infections in the presence of S. aureus and their effect in Skin Cutaneous Melanoma infections. GEO with accession number (GSE207390) was used to acquire the data. The microarray test was used to perform this investigation. Six sets of keratinocytes, IL-17A, and TNF-α were cultivated together. Several kinds of bioinformatics tools were employed to fulfill the study's objective. Gene hub analysis of 34284 genes was scanned. Six genes demonstrated high expression rates were expressed during the metastatic stage: , , , , , and . and had the highest levels of expression. The expression of the gene rose in response to sun exposure, but the expression of the other genes remained same. The existence of cytokine groups with in keratinocytes influences the expression difference compared to the other groups. This work adds to our understanding of the molecular alterations that occur in the epidermis of psoriasis patients, as well as their relationship to comorbidities. - Source: PubMed
Ali-Adel DawoodMawj-Saddam Zabn - Atopic dermatitis (AD) is a prevalent inflammatory skin disease and a major source of disease burden in children. Biomarker studies in childhood AD span genetic, immune, microbial and metabolic domains, but prior reviews have often focused on single molecular layers, specific sample sites or clinical classification. As a result, the field lacks an integrated, systems-level synthesis that compares and contextualizes biomarkers across domains while clearly distinguishing evidence strength. The rapid growth of literature in this field also poses practical challenges for traditional manual review workflows. - Source: PubMed
Publication date: 2026/07/04
Lee Jia WeiLoo Evelyn X LChong Samuel SBan Kenneth H KLee Caroline G - Diabetic foot ulcers (DFU) are a major complication of diabetes, often driven by chronic inflammation. The role of specific inflammatory cytokines in DFU development is unclear due to challenges in observational studies. This study used a two-sample, bidirectional Mendelian randomization (MR) approach to assess the causal effects of 41 circulating inflammatory cytokines on DFU risk. Instrumental variables were selected based on genome-wide significance and linkage disequilibrium criteria. The primary analysis was inverse-variance weighted, with validation through enzyme-linked immunosorbent assay and real-time PCR in DFU patients and controls. Genetically predicted levels of CTACK (CCL27) and MIG (CXCL9) were linked to reduced DFU risk, with odds ratios of 0.538 for CTACK and 0.501 for MIG. Sensitivity analyses confirmed the robustness of the findings. Reverse MR analysis showed no causal relationship between DFU and these cytokines. Clinical validation revealed lower protein and mRNA levels of CTACK and MIG in DFU patients. This study provides evidence for a protective role of CTACK and MIG in DFU development, suggesting that they could serve as biomarkers or therapeutic targets for diabetic wound care. - Source: PubMed
Liu JianyiTan HaoLiu YanLu ZhentanZhong WeibingNiu Zehao - Pancreatic islets undergo coordinated cellular remodeling during obesity-induced insulin resistance. However, longitudinal changes across endocrine and non-endocrine compartments remain largely unexplored. We present a comprehensive high-resolution atlas using longitudinal single-cell RNA sequencing (scRNA-seq) and single-cell ATAC sequencing (scATAC-seq) on islets from C57BL/6 mice subjected to high-fat diet (HFD) feeding for 8, 16, and 24 weeks, along with age-matched controls on regular chow (RC). We mapped dynamic changes in islet cell composition and transcriptional states. Trajectory inference indicated diversification of beta-cell programs into adaptive and inflammatory states under HFD. Progression of insulin resistance induced shrinkage and transcriptional remodeling of glucagon-secreting alpha-cells, marked by upregulation of genes related to intracellular transport and oxidative stress, accompanied by the emergence of a polyhormonal alpha-cell subpopulation. Similarly, we identified delta-cell subpopulations exhibiting beta-like transcriptional signatures and polyhormonal identity under nutritional stress, suggesting adaptive delta-cell plasticity that may partially compensate for beta-cell loss during insulin resistance. The islet microenvironment exhibited robust expansion of proinflammatory M1 macrophages, reaching a plateau by 16 weeks of HFD, indicating niche saturation. Cell-cell communication analyses revealed disruption of key signaling pathways within endocrine and between endocrine and non-endocrine cells under HFD conditions. Notably, CCL27a-chemokine receptor signaling between beta-cells and M1 macrophages was significantly reduced in HFD islets, likely driven by reduced Ccl27a expression and chromatin accessibility in a distinct beta cell subpopulation, which we further validated using INS-1 cells exposed to HFD-like conditions. Comparative analysis with scRNA seq of human islets confirmed conserved stress signatures. Furthermore, genetic variants at the CCL27 locus were associated with increased T2D risk and HOMA-IR in human populations, establishing a novel link between beta-cell stress and systemic inflammation. This resource provides a hierarchical framework for understanding islet failure and identifies potential therapeutic nodes for type 2 diabetes. - Source: PubMed
Publication date: 2026/06/01
Singh SimranPavan Musale KrushnaBarella Luiz FTelang JayeshShree AjitaAgarwal ShrutiGoel AyushThaleshwari SaahibaWess JürgenZafar HamimPydi Sai Prasad - Vesicular cutaneous lupus erythematosus (VCLE) is a rare autoimmune disease in dogs and is considered the canine counterpart of human subacute cutaneous lupus erythematosus (SCLE). However, the molecular mechanisms underlying VCLE remain incompletely defined. - Source: PubMed
Publication date: 2026/05/11
Clifford TreasaW Stranahan LaurenJ Wiener DominiqueKeating M KellyLeon RenatoBanovic Frane