CDH5 polyclonal antibody (A01)
- Known as:
- CDH5 pab (anti-) (A01)
- Catalog number:
- H00001003-A01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CDH5 polyclonal antibody (A01)
Related genes to: CDH5 polyclonal antibody (A01)
- Gene:
- ABRAXAS2 NIH gene
- Name:
- abraxas 2, BRISC complex subunit
- Previous symbol:
- KIAA0157, FAM175B
- Synonyms:
- Em:AC068896.4, ABRO1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2017-04-27
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
- Gene:
- ARHGAP4 NIH gene
- Name:
- Rho GTPase activating protein 4
- Previous symbol:
- -
- Synonyms:
- KIAA0131, C1, p115, RhoGAP4, SrGAP4
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2015-09-11
- Gene:
- ARHGEF7 NIH gene
- Name:
- Rho guanine nucleotide exchange factor 7
- Previous symbol:
- -
- Synonyms:
- KIAA0142, PIXB, DKFZp761K1021, Nbla10314, DKFZp686C12170, BETA-PIX, COOL1, P85SPR, P85, P85COOL1, P50BP, PAK3, P50
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2016-10-05
- Gene:
- BCLAF1 NIH gene
- Name:
- BCL2 associated transcription factor 1
- Previous symbol:
- -
- Synonyms:
- KIAA0164, BTF
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2017-06-09
Related products to: CDH5 polyclonal antibody (A01)
Related articles to: CDH5 polyclonal antibody (A01)
- Oral squamous cell carcinoma (OSCC) is characterized by high aggressiveness. This study aims to elucidate the role of NDRG1 in the evolutionary heterogeneity and spatial microenvironmental remodelling of OSCC. By integrating bulk transcriptomics, single-cell RNA sequencing (scRNA-seq), and spatial transcriptomics (ST), complemented by in vivo and in vitro functional assays, we systematically explored the regulatory logic of the MSTRG.47889/miR-1299/NDRG1 axis. The MSTRG.47889/miR-1299/NDRG1 ceRNA regulatory axis was identified and validated, demonstrating its significant role in promoting OSCC proliferation and invasion while impairing cellular adhesion. Single-cell analysis revealed a significant expansion of the NDRG1-high subpopulation in tumour tissues, which drives cellular evolution along a pseudotime trajectory toward a partial epithelial-mesenchymal transition (p-EMT) and a high glycolytic state. Spatial transcriptomics analysis revealed that NDRG1 is highly expressed within 'hypoxia-metabolic' niches. Our integrative analysis suggests that these regions may coordinate with endothelial cells, highlighting a potential role for the ANGPTL4-CDH5 signalling axis in promoting a proangiogenic microenvironment. These findings provide preliminary insights into how NDRG1 serves as a pivotal regulator driving p-EMT and coordinating niche remodelling. NDRG1 serves as a pivotal regulator driving p-EMT and proangiogenic niche remodelling, representing a potential novel target for the diagnosis and treatment of OSCC. - Source: PubMed
Publication date: 2026/06/27
Feng LeiOu YiTian LinqingJiang WenjieZhang MinSheng Xun - Breast cancer (BC) and non-small cell lung carcinoma (NSCLC) are two of the most prevalent and lethal malignancies, with shared molecular alterations that could serve as biomarkers for diagnosis and therapy. We employed integrated bioinformatics approaches to identify common hub genes in both cancers by analyzing eight GEO transcriptomic datasets. The protein-protein interaction network revealed ten hub genes: five upregulated (TOP2A, CCNB1, CCNB2, MELK, and UBE2C) and five downregulated (CDH5, MMRN2, RAMP2, CCM2L, and CD36), which were validated through transcriptomic analyses. These genes were associated with key process such as cell-cycle regulation, DNA replication, angiogenesis, and endothelial integrity. Among the hub genes analyzed, significant survival associations were observed for selected genes in a cancer-type-specific manner, particularly for several upregulated hub genes in LUAD, whereas most hub genes showed no statistically significant association with overall survival. Molecular docking results demonstrated favorable interactions between WGX-50 and these targets, with the top vina scores indicating a strong binding affinity. Subsequent molecular dynamics simulations of WGX-50 with CD36 and MELK confirmed stable interactions, involving hydrogen bonds, hydrophobic interactions, and water bridges. These findings highlight the therapeutic potential of WGX-50 as a multitarget anticancer agent capable of modulating multiple signaling cascades. This Insilico study provides valuable insights into the development of targeted therapies for BC, NSCLC, and presents WGX-50 as a promising anticancer candidate. - Source: PubMed
Publication date: 2026/06/25
Farooq AdilRizwan MuhammadYousaf NumanImran MuhammadJin MengyuanYang YiliangWei Dongqing - Endothelial dysfunction is a critical determinant of sepsis-associated organ injury, often driven by its interaction with overactivated immune cells. Neutrophils, the dominant early responders in sepsis, contribute to endothelial barrier disruption, yet the underlying metabolic and epigenetic mechanisms remain poorly understood. Here, we observed elevated intracellular lactate levels in neutrophils from septic patients which correlated with organ dysfunction and systemic inflammatory markers. Mechanistically, lactate-induced histone H3K18 lactylation (H3K18la) enhanced (autophagy related 7) transcription, initiating a non-degradative, secretory autophagy program. This facilitated the extracellular release of IL1B/IL-1B (interleukin 1 beta), a key driver of endothelial dysfunction. Interference of lactate production, ATG7 expression or IL1B signaling alleviated endothelial dysfunction . , myeloid-specific deletion of the lactylation writer EP300/p300 (EP300 lysine acetyltransferase) mitigated pulmonary endothelial dysfunction and lung injury. Additionally, the stress-responsive transcription factor ATF4/CREB-2 (activating transcription factor 4) was found to directly interact with both EP300 and H3K18la, amplifying H3K18la-driven transcription. Our findings uncover a metabolically driven, epigenetically regulated secretory autophagy pathway in neutrophils that mediates endothelial dysfunction. Our study provides mechanistic insights into neutrophil-endothelial crosstalk in sepsis and identifies EP300, ATG7, and IL1B as potential therapeutic targets for sepsis. ALI: acute lung injury; ANOVA: analysis of variance; ATF4/CREB-2: activating transcription factor 4; ATG7/GSA7: autophagy related 7; ATP: adenosine triphosphate; BafA1: bafilomycin A; BMDN: bone marrow-derived neutrophil; C-CASP1: cleaved-caspase 1; CDH5/CD144: cadherin 5; CRP/PTX1: C-reactive protein; CST3: cystatin C; CXCL8/IL-8: C-X-C motif chemokine ligand 8; DAPI: 4',6-diamidino-2-phenylindole; DEG: differentially expressed gene; dHL-60: dimethyl sulfoxide-differentiated HL-60 cell; DMSO: dimethyl sulfoxide; ELISA: enzyme-linked immunosorbent assay; EP300/p300: EP300 lysine acetyltransferase; GOT1/AST: glutamic-oxaloacetic transaminase 1; GPT/ALT: glutamic - pyruvic transaminase; GSDMD-N: gasdermin D N-terminal; H&E: hematoxylin and eosin; H3K18la: histone H3K18 lactylation; HRP: horseradish peroxidase; ICU: intensive care unit; IHC: immunohistochemistry; IL1B/IL-1B: interleukin 1 beta; IL1R1/CD121A: interleukin 1 receptor type 1; IL6/IL-6: interleukin 6; KEGG: Kyoto Encyclopedia of Genes and Genomes; LAMP1/CD107a: lysosome associated membrane protein 1; LDHA: lactate dehydrogenase A; LPS: lipopolysaccharide; 3-MA: 3-methyladenine; NLRP3/NALP3: NLR family pyrin domain containing 3; PBS: phosphate-buffered saline; PCT: procalcitonin; PMN: peripheral neutrophils; Rapa: rapamycin; RNA-seq: RNA-sequencing; SERPINE1/PAI1: serpin family E member 1; SDS-PAGE: sodium dodecyl sulfate polyacrylamide gel electrophoresis; SOFA: Sequential Organ Failure Assessment; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TNF/TNF-alpha: tumor necrosis factor; panKla: pan-histone lactylation; VCAM1/CD106: vascular cell adhesion molecule 1. - Source: PubMed
Publication date: 2026/06/12
Li YinjiaozhiLi RanranZhu DehaoTian RuiChen YangWang XiaoliLi LeiPan TingtingTan RuomingQu Hongping - Ischemic stroke remains a leading cause of disability and mortality worldwide, with limited acute therapeutic options. Sphingosine-1-phosphate (S1P) is a bioactive lipid that regulates endothelial function, vascular integrity, and immune responses, and reduced circulating S1P levels have been reported in ischemic stroke. Whether plasma S1P depletion parallels alterations in brain-endothelial S1P metabolism, receptor expression, and endothelial activation, however, remains unclear. Here, we characterized circulating S1P levels together with stroke-associated changes in brain-endothelial S1P pathway expression, markers related to endothelial activation, and blood-brain barrier (BBB) integrity. - Source: PubMed
Publication date: 2026/06/12
Porschen Lisa TMatthes FrankMatuskova HanaBraadt LinoPetzold Gabor CLindgren Arne GMeissner Anja - Carotid intima-media thickening (IMT) is a major risk factor for cardiovascular disease (CVD). The large ribosomal subunit protein 17 (Rpl17) was recently reported as a CVD-associated gene; however, ribosomal mutations generally are not associated with vascular dysfunction. We have created a novel genetic model of decreased RpL17 in endothelial cells (EC) to determine how changes in endothelial ribosome expression cause IMT. - Source: PubMed
Publication date: 2026/05/25
Wines-Samuelson MaryChowdhury SayantaniSenchanthisai SharonShaposhnikov MichalSowden MarkBerk Bradford C