Salt _ Binding _ Synonym BCNP SumFormula C13H17N3O6S2
- Known as:
- Salt _ Binding _ Synonym BCNP SumFormula C13H17N3O6S2
- Catalog number:
- A-2825.0001
- Product Quantity:
- 1.0 g
- Category:
- -
- Supplier:
- Bach
- Gene target:
- Salt _ Binding Synonym BCNP SumFormula C13H17N3O6S2
Related genes to: Salt _ Binding _ Synonym BCNP SumFormula C13H17N3O6S2
- Gene:
- NIBAN3 NIH gene
- Name:
- niban apoptosis regulator 3
- Previous symbol:
- FAM129C
- Synonyms:
- FLJ39802, BCNP1
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2006-11-23
- Date modifiied:
- 2019-04-18
Related products to: Salt _ Binding _ Synonym BCNP SumFormula C13H17N3O6S2
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody((Cys31,Nva34)_Neuropeptide Y (27_36))2 Salt _ Binding (Disulfide_bond) Synonym SumFormula C116H186N36O28S2((Cys31,Nva34)_Neuropeptide Y (27_36))2 Salt _ Binding (Disulfide_bond) Synonym SumFormula C116H186N36O28S2(+)-(2S,5R)-1-Allyl-2,5-dimethylpiperazine, (+)-Camphoric Acid Salt C19H34N2O4 CAS: 186094-00-8(+)-(2S,5R)-1-Allyl-2,5-dimethylpiperazine, (+)-Camphoric Acid Salt CAS: 186094-00-8 Formula: C19H34N2O4(+)-Biotin 4-Amidobenzoic Acid, Sodium Salt C17H20N3NaO4S CAS: 102418-74-6(+)-Biotin 4-Amidobenzoic Acid, Sodium Salt CAS: 102418-74-6 Formula: C17H20N3NaO4S(+)-Tianeptine Monosodium Salt C21H24ClN2NaO4S CAS: 169293-32-7(+)-Tianeptine Monosodium Salt CAS: 169293-32-7 Formula: C21H24ClN2NaO4S(+)_3_Bromocamphor_8_sulfonic acid ammonium Salt(+)_Dipara tolouyl_d_tartaric acid salt of 4_(+)_Usnic acid sodium salt Usnic acid sodium salt(+__)_3_Methyl_2_oxovaleric acid Sodium salt(-)-Tianeptine Monosodium Salt C21H24ClN2NaO4S CAS:(-)-Tianeptine Monosodium Salt CAS: Formula: C21H24ClN2NaO4S Related articles to: Salt _ Binding _ Synonym BCNP SumFormula C13H17N3O6S2
- Curcumin, a major phytochemical derived from Curcuma longa, has been shown to enhance the efficacy of chemotherapeutic agents such as doxorubicin, 5-fluorouracil, and cisplatin by overcoming drug resistance, making it a promising adjunct in the treatment of glioblastoma. However, the global gene-expression changes triggered by curcumin in glioblastoma remain underexplored. In this study, we investigated the effects of curcumin on human glioblastoma (U87 MG) cells, where it significantly reduced cell viability and proliferation in a dose- and time-dependent manner and induced apoptosis without affecting senescence. Transcriptomic analysis revealed 5036 differentially expressed genes, with pathway enrichment identifying 13 dysregulated cancer-associated pathways. Notably, curcumin modulated several key regulators involved in MAPK, Ras, TGF-β, Wnt, Cytokine, and TNF signaling pathways. Several apoptosis and cell cycle-associated genes, including PRKCG, GDF7, GDF9, GDF15, GDF5, FZD1, FZD2, FZD8, AIFM3, TP53AIP1, CRD14, NIBAN3, BOK, BCL2L10, BCL2L14, BNIPL, FASLG, GZMM, TNFSF10, TNFSF11, and TNFSF4, were significantly altered. Several pro-apoptotic and anti-BCL, cell-cycle-regulated genes were modulated following curcumin treatment, emphasizing its potential role in curcumin-mediated anti-tumor effects. This study provides insight into the molecular mechanisms underlying curcumin's action against glioblastoma. - Source: PubMed
Publication date: 2025/05/09
Mashozhera Nicole TendayiReddy Chinreddy SubramanyamRanasinghe Yevin NenukaNatarajan PurushothamanReddy Umesh KHankins Gerald - Idiopathic pulmonary fibrosis (IPF) is a severe interstitial lung disease characterized by a grim prognosis, in which various forms of cell death are significant contributors to its development. The objective of this study is to explore diagnostic biomarkers and molecular subtypes associated with PANoptosis in IPF, and to develop reliable diagnostic models based on PANoptosis-related mechanisms. The peripheral blood transcriptomic data of IPF from the Gene Expression Omnibus (GEO) database and PANoptosis-related genes from the GeneCards database were utilized to conduct differential gene expression analysis and weighted gene co-expression network analysis (WGCNA), identifying PANoptosis-related differentially expressed genes (PDEGs). We yielded 9 PDEGs and employed machine learning algorithms to identify 3 key diagnostic biomarkers for PANoptosis in IPF: MMP9, FCMR, NIBAN3. Consensus clustering algorithm was applied to recognize two PANoptosis-related subtypes. Cluster 1 exhibited higher abundance of adaptive immune response cells and significant enrichment in DNA damage and repair-related pathways. Cluster 2 exhibited greater prevalence of innate immune response cells and predominant enhancement in pathways related to lipid cholesterol metabolism and vascular remodeling. Diagnostic models were developed with the aid of clinical decision-making and a novel approach to the diagnosis and treatment for IPF. - Source: PubMed
Publication date: 2024/10/14
Wu LiLiu YangZhang YifanXu RuiBi KaixinLi JingWang JiaLiu YabingGuo WanjinWang QiChen Zhiqiang - Interactions between the products of the nuclear and mitochondrial genomes are critical for the function of most eukaryotic cells. Recently the introduction of mitochondrial replacement therapy has raised the question of incompatibilities between mitochondrial and nuclear variants, and their potential influence on the genetic makeup of human populations. Such interactions could also contribute to the variability of the penetrance of pathogenic DNA variants. This led us to investigate the frequencies of combinations of nuclear and mitochondrial SNP alleles (mitonuclear combinations) in healthy individuals (n = 5375) and in a cohort of patients with Parkinson's disease (PD, n = 2210). In the unaffected population, we were not able to find associations between nuclear and mitochondrial variants with a false discovery rate below 0.05 after accounting for multiple testing (i.e., the number of combinations examined). However, in the PD cohort, five combinations surpassed this threshold. Next, after combining both cohorts, we investigated whether these associations were modulated by disease status. All five combinations were significant (p < 10 for all tests). These combinations also showed significant evidence for an effect of the interaction between the mitochondrial and nuclear variants on disease risk. Their nuclear components mapped to TBCA, NIBAN3, and GLT25D1 and an uncharacterised intergenic region. In summary, starting from a single cohort design we identified combinations of nuclear and mitochondrial variants affecting PD disease risk. - Source: PubMed
Publication date: 2022/02/12
Pickett Sarah JDeen DashaPyle AngelaSantibanez-Koref MauroHudson Gavin - B-cell novel protein-1 (BCNP1) or Family member of 129C (FAM129C) was identified as a B-cell-specific plasma-membrane protein. Bioinformatics analysis predicted that BCNP1 might be heavily phosphorylated. The BCNP1 protein contains a pleckstrin homology (PH) domain, two proline-rich (PR) regions and a Leucine Zipper (LZ) domain suggesting that it may be involved in protein-protein interactions. Using The Cancer Genome Atlas (TCGA) data sets, we investigated the correlation of alteration of the BCNP1 copy-number changes and mutations in several cancer types. We also investigated the function of BCNP1 in cellular signalling pathways. We found that BCNP1 is highly altered in some types of cancers and that BCNP1 copy-number changes and mutations co-occur with other molecular alteration events for TP53 (tumour protein P53), PIK3CA (Phosphatidylinositol-4,5-Bisphosphate 3-Kinase, Catalytic Subunit Alpha), MAPK1 (mitogen-activated protein kinase-1; ERK: extracellular signal regulated kinase), KRAS (Kirsten rat sarcoma viral oncogene homolog) and AKT2 (V-Akt Murine Thymoma Viral Oncogene Homolog 2). We also found that PI3K (Phoshoinositide 3-kinase) inhibition and p38 MAPK (p38 mitogen-activated protein kinase) activation leads to reduction in phosphorylation of BCNP1 at serine residues, suggesting that BCNP1 phosphorylation is PI3K and p38MAPK dependent and that it might be involved in cancer. Its degradation depends on a proteasome-mediated pathway. - Source: PubMed
Publication date: 2016/09/29
Patel Sapan JTrivedi Gaurang LDarie Costel CClarkson Bayard D - We applied a unique method to identify genes expressed in whole blood that can serve as biomarkers to detect colorectal cancer (CRC). - Source: PubMed
Publication date: 2008/01/18
Han MarkLiew Choong TsekZhang Hong WeiChao SamuelZheng RunYip Kok ThyeSong Zhen-YaLi Hiu MingGeng Xiao PingZhu Li XinLin Jian-JiangMarshall K WayneLiew Choong Chin