MAPK3 & CASP9 Protein Protein Interaction Antibody Pair
- Known as:
- MAPK3 & CASP9 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0013
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MAPK3 & CASP9 Protein Interaction Antibody Pair
Related genes to: MAPK3 & CASP9 Protein Protein Interaction Antibody Pair
- Gene:
- CASP9 NIH gene
- Name:
- caspase 9
- Previous symbol:
- -
- Synonyms:
- MCH6, ICE-LAP6, APAF-3, PPP1R56
- Chromosome:
- 1p36.21
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-11
- Date modifiied:
- 2016-04-25
- Gene:
- MAPK3 NIH gene
- Name:
- mitogen-activated protein kinase 3
- Previous symbol:
- PRKM3
- Synonyms:
- ERK1, p44mapk, p44erk1
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2015-09-03
Related products to: MAPK3 & CASP9 Protein Protein Interaction Antibody Pair
Related articles to: MAPK3 & CASP9 Protein Protein Interaction Antibody Pair
- To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - Recent studies link pesticide exposures to cardiovascular disease risk factors. However, research on the combined effects of multiple pesticides on atherosclerotic cardiovascular disease (ASCVD) is limited, particularly in rural areas. Despite advances in toxicogenomics, the mechanisms underlying these effects remain unclear. This study aims to investigate the combined effects and mechanisms of pesticide exposures on ASCVD. - Source: PubMed
Publication date: 2024/12/10
Wu XueyanWei DandanZhou YilinCao QingqingHan GuozhenHan ErbaoChen ZhiweiGuo YaoHuo WenqianWang ChongjianHuang ShanZeng XinWang XinluMao Zhenxing - Non-small cell lung cancer (NSCLC) is one of the leading causes of human death worldwide. Herbal prescription SH003 has been developed to treat several cancers including NSCLC. Due to the multi-component nature of SH003 with multiple targets and pathways, a network pharmacology study was conducted to analyze its active compounds, potential targets, and pathways for the treatment of NSCLC. - Source: PubMed
Publication date: 2024/02/01
Lee KangwookChoi Yu-JeongLim Hae-InCho Kwang JinKang NuriKo Seong-Gyu - The fungal toxin aflatoxin B1 (AB1) and its reactive intermediate, aflatoxin B1-8, 9 epoxide, could cause liver cancer by inducing DNA adducts. AB1 exposure can induce changes in the expression of several cancer-related genes. In this study, the effect of AB1 exposure on breast cancer MCF7 and normal breast MCF10A cell lines at the phenotypic and epigenetic levels was investigated to evaluate its potential in increasing the risk of breast cancer development. We hypothesized that, even at low concentrations, AB1 can cause changes in the expression of important genes involved in four pathways, i.e., p53, cancer, cell cycle, and apoptosis. The transcriptomic levels of , , , , , , , , , , , , , , and were determined in MCF7 and MCF10A cells. Our results illustrate that treating both cells with AB1 induced cytotoxicity and apoptosis with reduction in cell viability in a concentration-dependent manner. Additionally, AB1 reduced reactive oxygen species levels. Phenotypically, AB1 caused cell-cycle arrest at G1, hypertrophy, and increased cell migration rates. There were changes in the expression levels of several tumor-related genes, which are known to contribute to activating cancer pathways. The effects of AB1 on the phenotype and epigenetics of both MCF7 and MCF10A cells associated with cancer development observed in this study suggest that AB1 is a potential risk factor for developing breast cancer. - Source: PubMed
Publication date: 2022/10/06
Adam Mowaffaq Adam AhmedKamal Laina Zarisa MuhdKanakal MahibubBabu DineshDahham Saad SabbarTabana YasserLok BronwynBermoy Brittany MYunus Muhammad AmirThan Leslie Thian LungBarakat KhaledSandai Doblin - . Infantile hemangiomas may have unexpected behavior. Initial regression (spontaneously or drug-induced) may be followed by unexplained recurrences. At this moment, there are no well-established criteria to predict infantile hemangioma reccurrences. . We compared the VEGF pathway gene expression profile for one case of involuting infantile hemangioma versus one case of recurrent proliferative infantile hemangioma using TaqMan Array. . We found ten genes upregulated for both involuting and recurrent proliferative hemangiomas: ACTB, KRAS, MAP2K1, HRAS, NOS3, BAD, HSPB1, HPRT1, GUSB, and CASP9. Thirteen genes were downregulated for both involuting and proliferative hemangiomas: FIGF, ACTG1, GRB2, MAPKAPK2, ACTG2, MAP2K2, MAPK3, HSP90AA1, MAP2K6, NRAS, ACTA1, KDR, and MAPK1. Three genes showed divergent expression between proliferating and involuting hemangiomas. Proliferating hemangioma had MAPK14 and AKT1 gene upregulation and ACTA2 downregulation. Involuting infantile hemangioma was characterized by ACTA2 upregulation and AKT1 and MAPK14 downregulation. . Three genes, AKT1, p38/MAPK14, and ACTA2, were found to have divergent expression in proliferating and involuting infantile hemangiomas. Excepting AKT1, which was mentioned in the last ISSVA classification (strictly related to Proteus Syndrome), none of the other genes were reported. An accurate gene expression profile mapping of infantile hemangiomas together with a gene expression-based hemangioma classification is stringently needed. - Source: PubMed
Publication date: 2022/06/17
Heredea Rodica ElenaMelnic EugenCirligeriu Laura ElenaBerzava Patricia LorenaStănciulescu Maria CorinaPopoiu Călin MariusCimpean Anca Maria