ADAM8 ELISA kit
- Known as:
- ADAM8 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADAM8-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADAM8 ELISA kit
Ask about this productRelated genes to: ADAM8 ELISA kit
- Gene:
- ADAM8 NIH gene
- Name:
- ADAM metallopeptidase domain 8
- Previous symbol:
- -
- Synonyms:
- CD156, MS2, CD156a
- Chromosome:
- 10q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-13
- Date modifiied:
- 2015-08-24
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- New targeted treatments are urgently needed to improve triple-negative breast cancer (TNBC) patient survival. Previously, we identified the cell surface protein A Disintegrin And Metalloprotease 8 (ADAM8) as a driver of TNBC tumor growth and spread via its metalloproteinase and disintegrin (MP and DI) domains. In proof-of-concept studies, we demonstrated that a monoclonal antibody (mAb) that simultaneously inhibits both domains represents a promising therapeutic approach. Here, we screened a hybridoma library using a multistep selection strategy, including flow cytometry for Ab binding to native conformation protein and in vitro cell-based functional assays to isolate a novel panel of highly specific human ADAM8 dual MP and DI inhibitory mAbs, called ADPs. The screening of four top candidates for in vivo anti-cancer activity in an orthotopic MDA-MB-231 TNBC model of ADAM8-driven primary growth identified two lead mAbs, ADP2 and ADP13. Flow cytometry, hydrogen/deuterium exchange-mass spectrometry (HDX-MS) and alanine (ALA) scanning mutagenesis revealed that dual MP and DI inhibition was mediated via binding to the DI. Further testing in mice showed ADP2 and ADP13 reduce aggressive TNBC characteristics, including locoregional regrowth and metastasis, and improve survival, demonstrating strong therapeutic potential. The continued development of these mAbs into an ADAM8-targeted therapy could revolutionize TNBC treatment. - Source: PubMed
Publication date: 2024/04/13
Mineva Nora DPianetti StefaniaDas Sonia GSrinivasan SrimathiBilliald Nicolas MSonenshein Gail E - TNFAIP8 and TIPE2 belong to TNFa-induced protein 8 (TNFAIP8/TIPE) family. They control apoptosis and direct leukocyte migration. Nucleus pulposus (NP) cell loss is a hallmark of intervertebral disc (IVD) degeneration in response to injury, and inflammation may cause pain. Here, we examined the effects of TNFAIP8/TIPE2 deficiency on the IVDs in mice with these genes deleted. - Source: PubMed
Publication date: 2024/04/09
Lu JiaweiTian ZuozhenShofer Frances SQin LingSun HonghongZhang Yejia - Temporal lobe epilepsy (TLE) is one of the most common forms of focal epilepsy. Levetiracetam (LEV) is an antiepileptic drug whose mechanism of action at the genetic level has not been fully described. Therefore, the aim of the present work was to evaluate the relevant gene expression changes in the dentate gyrus (DG) of LEV-treated rats with pilocarpine-induced TLE. Whole-transcriptome microarrays were used to obtain the differential genetic profiles of control (CTRL), epileptic (EPI), and EPI rats treated for one week with LEV (EPI + LEV). Quantitative RT-qPCR was used to evaluate the RNA levels of the genes of interest. According to the results of the EPI vs. CTRL analysis, 685 genes were differentially expressed, 355 of which were underexpressed and 330 of which were overexpressed. According to the analysis of the EPI + LEV vs. EPI groups, 675 genes were differentially expressed, 477 of which were downregulated and 198 of which were upregulated. A total of 94 genes whose expression was altered by epilepsy and modified by LEV were identified. The RT-qPCR confirmed that LEV treatment reversed the increased expression of mRNA and decreased the expression of the , , , and genes in the DG. These results indicate that LEV could be involved in nonclassical mechanisms involved in Ca homeostasis and the regulation of the mTOR pathway through , , , , and , contributing to reduced hyperexcitability in TLE patients. - Source: PubMed
Publication date: 2024/01/30
Diaz-Villegas VeronicaPichardo-Macías Luz AdrianaJuárez-Méndez SergioIgnacio-Mejía IvánCárdenas-Rodríguez NoemíVargas-Hernández Marco AntonioMendoza-Torreblanca Julieta GriseldaZamudio Sergio R - Colorectal cancer (CRC) is one of the most prevalent and deadliest illnesses all around the world. Growing proofs demonstrate that tumor-associated macrophages (TAMs) are of critical importance in CRC pathogenesis, but their mechanisms remain yet unknown. The current research was designed to recognize underlying biomarkers associated with TAMs in CRC. We screened macrophage-related gene modules through WGCNA, selected hub genes utilizing the LASSO algorithm and COX regression, and established a model. External validation was performed by expression analysis using datasets GSE14333, GSE74602, and GSE87211. After validating the bioinformatics results using real-time quantitative reverse transcription PCR, we identified SPP1, C5AR1, MMP3, TIMP1, ADAM8 as potential biomarkers associated with macrophages in CRC. - Source: PubMed
Publication date: 2024/02/02
Lin DongfaZheng TingjinHuang ShangyuanLiu RuiGuan ShuwenZhang Zhishan - - Source: PubMed
Publication date: 2023/08/02
Tian ZuozhenShofer Frances SFan MingyueSandroni Alec ZYao LutianHan LinQin LingEnomoto-Iwamoto MotomiZhang Yejia