SDF-1a (Mouse) recombinant proteins
- Known as:
- SDF-1a (Mouse) Rec. proteins
- Catalog number:
- rAP-0061-2
- Product Quantity:
- 2.00 ug
- Category:
- -
- Supplier:
- AngoiPro
- Gene target:
- SDF-1a (Mouse) recombinant proteins
Related products to: SDF-1a (Mouse) recombinant proteins
Related articles to: SDF-1a (Mouse) recombinant proteins
- The recent study aims to analyze the role of non-coding RNAs, particularly circRNAs, in HIV pathogenesis using construction of immune-related regulatory networks. In compliance with ethical standards and institutional guidelines, publicly available HIV-related mRNA and microRNA expression datasets were systematically retrieved from the Gene Expression Omnibus repository. These datasets underwent rigorous bioinformatics analysis employing the "limma" package in R to identify differentially expressed genes (DEGs) and microRNAs (DEmiRNAs). Validated interaction data from miRBase and ENCORI databases facilitated the construction of circRNA-DEmiRNA and DEmiRNA-DEG regulatory networks. Protein-protein interaction networks were generated through STRING database analysis, with hub genes defined as those within the highest 5% of interaction degrees. Furthermore, single-cell RNA sequencing (scRNA-seq) datasets from HIV-infected individuals were analyzed using the "Seurat" package to identify DEGs in CD4+ and CD8+ T cell subsets. Cross-validation between microarray and scRNA-seq data ensured robustness of identified hub genes. Our results revealed substantial alterations in RNA expression associated with both high viral load and low viral load HIV infections. Single-cell analyses indicated significant gene expression shifts in T cell populations: 194 upregulated and 813 downregulated genes in CD4+ T cells, and 244 upregulated and 567 downregulated genes in CD8+ T cells. Integrated analysis delineated five hub genes consistently dysregulated across T cell subsets. STAT1 and DDX39B were upregulated, whereas CXCL8, CXCL12, and PTGS2 were downregulated. The pathway enrichment analysis indicated that these genes are implicated in key regulatory pathways relevant to infectious disease mechanisms. Alongside of DEGs, our studies indicated that multiple miRNAs, such as hsa-miR-21-5p, hsa-miR-146a-5p and hsa-let-7b-5p are differentially expressed in HIV-infected samples in comparison to the normal samples. Afterward, DEmiRNA-DEGs network studies demonstrated different axes between significantly up- and down-regulated DEGs with down- and up-regulated miRNAs, respectively. Following, ceRNA regulatory network revealed circRNAs, which can interact with DEmiRNA-DEGs networks, like hsa_circ_0089761-hsa-miR-21-5p-CXCL12, hsa_circ_0003812-hsa-miR-146a-5p-PTGS2, and has_circ_0007185-has_let-7b-5p-DDX39B. Overall, this integrative analysis suggests potential circRNA-mediated regulatory mechanisms in HIV infection and highlights potential candidate circRNAs that may serve as biomarkers or therapeutic targets for further investigation. - Source: PubMed
Publication date: 2026/08/14
Faraji NeginRouhi LeilaBolhassani AzamHasannejad-Asl BehnamBaesi KazemAbbasian Ladan - Platelets are considered intravascular effectors of hemostasis, yet growing evidence indicates that they can migrate across the endothelium. Whether platelet exit from the vasculature is a regulated process analogous to leukocyte trafficking and how migration is coordinated with effector functions has remained unclear. Using genetic, pharmacologic, and imaging approaches, we define the molecular program governing platelet transendothelial migration into tumors in vivo. CXCL12-CXCR4 signaling contributed to platelet extravasation in vivo, with stromal rather than tumor-derived CXCL12 acting as the dominant cue; CXCR4 disruption reduced platelet infiltration and tumor growth. Efficient vascular exit required platelet focal adhesion kinase and platelet endothelial cell adhesion molecule 1, implicating cytoskeletal remodeling and junctional adhesion. Platelet trafficking was uncoupled from effector activity: Munc13-4-dependent dense granule secretion was dispensable for extravasation but required for growth promotion, whereas Munc18-2-regulated α-granule release preserved vascular integrity and restricted passage. Disruption of the CLEC-2/podoplanin axis destabilized vessels and increased leakage. Together, these findings establish regulated platelet extravasation. - Source: PubMed
Publication date: 2026/06/19
Lee HaniCarlos Alcalde WendolynGonzalez Delgado RicardoAhn Ju YoungVasquez MatthewCho Min SoonWong Stephen T CSood Anil KAfshar-Kharghan Vahid - Acute myeloid leukemia (AML) is a highly aggressive hematologic malignancy in which inflammatory signaling plays a pivotal role in disease pathogenesis. The dysregulation of the cytokine network leads to an increased abundance of pro-inflammatory mediators, such as IL-1β, TNF-α and IL-6, relative to anti-inflammatory cytokines like TGF-β and CXCL12. This disbalance in cytokine levels is closely associated with tumor development and fosters a pro-tumorigenic microenvironment by facilitating leukemic cell proliferation, reducing survival rates, and promoting drug resistance. In addition, inflammatory cytokines have been shown to preferentially support hematopoietic stem and progenitor cell populations harboring mutations associated with clonal hematopoiesis. This review summarizes the current knowledge on inflammatory cytokines and signaling pathways in AML, focusing on: (i) their mechanisms of action and implications for immune tolerance and clonal hematopoiesis and (ii) the emerging therapeutic strategies targeting these pathways to improve clinical outcomes for patients with AML. - Source: PubMed
Publication date: 2026/08/08
Suls ToonLion EvaVan Oers FlorianDe Backer EvaLasorsa ElenaAnguille Sébastien - This study aimed to clarify the relationship between stromal cell‑derived factor 1 (SDF‑1) and osteoblast-related responses in periodontal ligament (PDL) during orthodontic tooth movement (OTM) after tooth extraction, based on the hypothesis that local inhibition of SDF‑1/C‑X‑C chemokine receptor type 4 (CXCR4) signaling with the CXCR4 antagonist AMD3100 would attenuate osteoblast differentiation and alveolar bone remodeling during OTM. - Source: PubMed
Hamada YoshiyukiIshida YujiHuang Albert Chun-ShuoHamahara KentaRintanalert DuangtawanLi KaiHatano-Sato KasumiHosomichi JunUsumi-Fujita RisaOno Takashi - The clinical significance of CXC ligand 12 (CXCL12) expression at the invasive front of pancreatic ductal adenocarcinoma (PDAC) remains unclear. This study examined the expression of stromal using RNAscope for direct visualization of RNA localization and compared expression profiles with clinicopathological findings. - Source: PubMed
Publication date: 2026/08/11
Imamura ShunsukeUehara TakeshiIwaya MaiAsaka ShihoSugenoya ShinsukeSawaguchi HiroshiYoshizawa TakahiroKuraishi YasuhiroNakajima TomoyukiKomamura ShotaroNakamura AkiraIwaya YugoShimizu AkiraSoejima YujiOta HiroyoshiNagaya Tadanobu