NFKBIA Antibody - N-terminal region (ARP30301_P050)
- Known as:
- NFKBIA Antibody - N-terminal region (ARP30301_P050)
- Catalog number:
- arp30301_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NFKBIA Antibody - N-terminal region (ARP30301_P050)
Related genes to: NFKBIA Antibody - N-terminal region (ARP30301_P050)
- Gene:
- NFKBIA NIH gene
- Name:
- NFKB inhibitor alpha
- Previous symbol:
- NFKBI
- Synonyms:
- IKBA, MAD-3, IkappaBalpha
- Chromosome:
- 14q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-13
- Date modifiied:
- 2019-04-23
Related products to: NFKBIA Antibody - N-terminal region (ARP30301_P050)
Related articles to: NFKBIA Antibody - N-terminal region (ARP30301_P050)
- Acne vulgaris is a chronic inflammatory disorder of the pilosebaceous unit and is associated with Cutibacterium acnes overgrowth, excessive sebum production, and persistent inflammatory responses. This study evaluated the anti-acne potential of the cell-free supernatant (CFS) from Lacticaseibacillus parahuelsenbergensis THGS-36 and investigated its host-modulatory effects in sebocytes with a focus on CREB-associated signaling. THGS-36 CFS exhibited dose-dependent antibacterial activity against C. acnes strains KACC 11946 and KACC 19884, with identical minimum inhibitory concentration and minimum bactericidal concentration values of 1.25 mg/mL, and inhibited biofilm formation beginning at a sub-inhibitory concentration. In human sebocytes, 50 μg/mL THGS-36 CFS reduced C. acnes adhesion by 17.2% and significantly suppressed C. acnes CFS-induced secretion of IL-1β, IL-6, IL-8, and TNF-α, concomitant with reduced expression of TLR2 and NFKBIA, as well as decreased phosphorylation of IκBα and p65, indicating attenuation of NF-κB signaling. Under IGF-1 stimulation, THGS-36 CFS decreased lipid accumulation and downregulated lipogenesis-associated transcripts, including SREBF1, FASN, and PPARG. Mechanistically, the anti-inflammatory and anti-lipogenic effects of THGS-36 CFS were associated with stimulus-dependent modulation of CREB phosphorylation. Whole-genome sequencing supported the safety profile of THGS-36 by revealing no detectable virulence- or antibiotic resistance-associated determinants and identifying putative class II bacteriocin gene clusters. Collectively, THGS-36 CFS exerts multi-target anti-acne activity by inhibiting C. acnes growth and biofilm formation while attenuating sebocyte inflammation and lipogenesis, supporting its potential as a safe adjuvant or alternative strategy for acne treatment. - Source: PubMed
Publication date: 2026/05/28
Zheng QiwenYi Gyeong-SeonBae Chan-IlKim SomyeongNguyen Trang Thi MinhKim Jae-WooKim Mi-JuYi Tae-Hoo - BackgroundBreast cancer is the leading cause of cancer-related mortality among women in developing nations. encodes the inhibitors of nuclear factor-kappaB (NF-κB), which plays a critical role in modulating inflammation and carcinogenic processes. However, no prior studies were conducted to determine the association between polymorphisms and breast cancer susceptibility in the Bangladeshi population. Therefore, we aimed to examine the association of the (rs696) polymorphism with breast cancer risk in Bangladeshi women.MethodsThis case-control study involved 168 breast cancer patients and 150 healthy volunteers, utilizing polymerase chain reaction-restriction fragment length polymorphism. We assessed the -value, odds ratio (OR), and 95% confidence interval (CI) to analyze the level of risk association of rs696.ResultsThe cancer patients exhibited a higher mutant allele frequency than the controls. Breast cancer patients who are carriers of the mutant allele demonstrated a markedly elevated risk in two genetic models, including the additive model 2 (GG vs. AA: OR = 2.09, 95% CI = 1.03-4.23, -value=0.042) and the dominant model (AG + GG vs. AA: OR = 1.73, 95% CI = 1.07-2.78, -value=0.025). Moreover, the analysis of allele frequency indicated that carriers of the mutant allele G among breast cancer patients exhibited a significantly elevated risk compared to carriers of the wild-type A allele (G vs. A: OR = 1.42, 95% CI = 1.04-1.96, -value=0.029).ConclusionOur results suggest that (rs696) might be associated with an increased risk of breast cancer in Bangladeshi women. However, we recommend studies in the future with a larger sample size to validate these findings. - Source: PubMed
Publication date: 2026/05/29
Meem Sara ShahidKhan Sakif AhamedBhuiyan Mohiuddin AhmedIslam Mohammad SafiqulIslam Md RezaulMazid Md AbdulDewan Syed Masudur Rahman - Necrotizing enterocolitis (NEC), a life-threatening neonatal gastrointestinal disease, lacks reliable biomarkers. This study explores PANoptosis-a novel inflammatory cell death pathway-in NEC pathogenesis. - Source: PubMed
Publication date: 2026/05/27
Jia Li-LiLuo Shu-YueYe Xiao-YaZhu Hong-HongLi Zhan-Li - To elucidate the neuroimmune regulatory mechanism of the circadian rhythm gene KLF10 as a biomarker for anxiety depressive disorder (ADD). - Source: PubMed
Liu AnlanGuo WeifengLi JianxiangZhang TiangeXu Dan - Coronavirus Disease 2019 (COVID-19) and other lower respiratory tract diseases (LRTDs), including bacterial pneumonia and acute respiratory distress syndrome, share overlapping clinical features but arise from distinct pathophysiological mechanisms. The molecular signatures that distinguish these diseases remain insufficiently characterized in African populations, where genetic background, endemic infections, and environmental exposures may substantially shape immune responses. We integrated spatially resolved single-cell transcriptomic profiles from lung autopsy specimens of 30 Malawian patients, including 10 with COVID-19, 12 with other LRTDs, and 8 non-LRTD controls. In total, 61,391 cells representing 15 cell types and 36,602 gene expression features were analyzed. Using an integrated machine learning framework that combined nine feature-ranking algorithms with incremental feature selection, we identified potential molecular signatures that could discriminate among disease states within this cohort. The optimal classification models achieved weighted F1 scores greater than 0.94, demonstrating a robust capacity to differentiate COVID-19 from other LRTDs in our dataset. Notably, the macrophage-associated state in COVID-19 was dominated by an IFN-γ response with upregulation of CD163 and HLA-DQA2, contrasting sharply with the type I/III interferon signature reported in European cohorts. In addition, we observed cell-type-specific COVID-19 signatures, including downregulation of CAV1 in AT1 cells, consistent with epithelial damage; dysregulation of SFTPC in AT2 cells, suggesting surfactant dysfunction; and upregulation of NFKBIA in neutrophils, indicating altered inflammatory regulation. Gene Ontology enrichment further revealed universal disruption of protein synthesis machinery, along with cell-type-specific alterations in immune activation, epithelial repair, and inflammatory signaling pathways. - Source: PubMed
Publication date: 2026/05/04
Bao YushengZhou XianchaoChen LeiFeng KaiyanGuo WeiHuang TaoCai Yu-Dong