FGD1 siRNA_Lentivectors
- Known as:
- FGD1 siRNA_Lentivectors
- Catalog number:
- i007877d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FGD1 siRNA_Lentivectors
Related genes to: FGD1 siRNA_Lentivectors
- Gene:
- FGD1 NIH gene
- Name:
- FYVE, RhoGEF and PH domain containing 1
- Previous symbol:
- FGDY
- Synonyms:
- ZFYVE3
- Chromosome:
- Xp11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: FGD1 siRNA_Lentivectors
Related articles to: FGD1 siRNA_Lentivectors
- The success of modern drug-resistant tuberculosis (DR-TB) regimens increasingly depends on linezolid (LZD) and pretomanid (Pa), yet the emergence of resistance to these critical agents threatens to reverse recent treatment advances, with limited consolidated evidence available from high-burden settings such as South Africa. - Source: PubMed
Publication date: 2026/05/28
Kaapu Kabelo GabrielMakondo Vukosi TreasureCosta Conceição EmilynRukasha Ivy - Familial glucocorticoid deficiency (FGD) is a rare autosomal recessive disorder characterized by isolated cortisol deficiency and elevated adrenocorticotropic hormone (ACTH) levels. Variants in , which encodes mitochondrial thioredoxin reductase 2, have recently been implicated in FGD; however, the phenotypic and mutational spectrum remain extremely limited. - Source: PubMed
Publication date: 2026/05/28
Al Alwan IbrahimAlhamoudi Kheloud MAlzaben Abdullah IbrahimAlmulhem BeshaierQawasmi NawalAlswailem MeshaelAlotaibi SaraAlsaihati BurairJabaan AmjadMahzari MoeberFlück Christa EAlzahrani Ali S - Asthma is a chronic respiratory disease affecting over 230 million people worldwide, with higher prevalence in women. Environmental allergens such as house dust mite (HDM) trigger airway inflammation and hyperresponsiveness (AHR), yet the epigenetic mechanisms underlying these responses remain poorly understood. Furthermore, the role of estrogen receptors in the context of asthma is understudied. We aimed to investigate whether estrogen receptor-specific DNA methylation contributes to HDM-induced airway remodeling and hyperresponsiveness. Male and female C57BL/6J wild-type mice and estrogen receptor α and β knockout mice (Esr1 and Esr2) were exposed to HDM or phosphate-buffered saline for five weeks. DNA methylation and RNA sequencing data were obtained from snap-frozen whole lung tissues. HDM exposure resulted in widespread differential methylation of genes associated with inflammation and AHR, including . Notably, the absence of estrogen receptor β (in Esr2 mice) produced the most pronounced methylation patterns, particularly in females. Pathway enrichment analysis revealed asthma-relevant processes such as extracellular matrix remodeling, leukocyte adhesion and migration, airway smooth muscle contraction, and inflammatory signaling. Integration of methylation and gene expression data confirmed significant correlations (p<0.05) for , , and , and a marginal correlation for Chst7 (p<0.1), implicating these genes in allergic asthma pathogenesis. Our findings demonstrate that HDM exposure induces sex-specific epigenetic changes mediated by estrogen receptor status, highlighting a potential mechanism for increased asthma susceptibility in women. These results can inform estrogen receptor-targeted treatment strategies for allergic airway diseases. - Source: PubMed
Publication date: 2026/06/12
Commodore SarahEkpruke Carolyn DamilolaAlford RachelBorges-Sosa Omar AlejandroRousselle DustinBabayev MaksatIgwe ChukwudikeHemmerich Christopher MRusch Douglas BSilveyra Patricia - Tuberculosis (TB) remains a major global health problem, and treatment progress is increasingly threatened by rising multidrug-resistant tuberculosis (MDR-TB). Delamanid (DLM), a nitroimidazole drug, has shown good efficacy and safety against both drug-susceptible and drug-resistant () strains. However, data on its resistance mechanisms, drug susceptibility testing (DST), clinical effectiveness, safety, and pharmacokinetics remain limited. This review aims to summarize the most recent molecular, structural, and clinical evidence related to DLM. - Source: PubMed
Publication date: 2026/05/04
Islam Md MahmudulHasan Md ZahidTusar Md Touki TahamidHossain Md YeaminHossain Md MotaherJubayed Md Abdulla AlJubaer-Al-Abedin MdSoikot SheikhAkther ShanzidaBhuyian JahidGazi Hafizur RahmanHasan B M MahmudulAzam Md ShofiulHaque Md EnamulAbdullah-Al-Jubayer Hasan Md FarukHaydar F M AliKhalekuzzaman MdIslam Md TorequlHasan Sohel - MDR TB treatment is now facing the perils of emerging resistance to BDQ(bedaquiline) and DLM(delaminid). Both DLM and PRT(pretomanid) belong to the nitroimidazole group of drugs. Drug resistance in Mycobacterium Tuberculosis (MTB) is an ever changing, continuous and evolving process whereby the bacteria finds new genetic mutations to escape destruction by the newer drugs. DLM and PRT belong to the same class of drugs and resistance to both drugs have been described with mutations in five M. tuberculosis genes (ddn, fgd1, fbiA, fbiB, and fbiC) resulting in very high level of cross-resistance between the two drugs. Mutations in Rv2983 (fbiD), fbiB genes and some ddn allelles (S78Y, Y133C) can cause resistance to PRT but the strains may retain susceptibility to DLM. These reasons may lead to slight preference for DLM as compared to PRT. Such implications may be also kept in mind while treatment of MDR-TB with DLM and PRT. - Source: PubMed
Publication date: 2025/09/20
Sharma AmitChatterjee PoulomiShastry Shashank