ABCA2 Pre-design Chimera RNAi
- Known as:
- ABCA2 Pre-design Chimera RNAi
- Catalog number:
- H00000020-R03
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ABCA2 Pre-design Chimera RNAi
Related genes to: ABCA2 Pre-design Chimera RNAi
- Gene:
- ABCA2 NIH gene
- Name:
- ATP binding cassette subfamily A member 2
- Previous symbol:
- ABC2
- Synonyms:
- -
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-16
- Date modifiied:
- 2016-10-05
Related products to: ABCA2 Pre-design Chimera RNAi
Related articles to: ABCA2 Pre-design Chimera RNAi
- Vitamin D deficiency is a recognized risk factor for multiple sclerosis (MS), yet the molecular mechanisms linking vitamin D3 supplementation to immune regulation remain incompletely understood. - Source: PubMed
Publication date: 2026/07/31
Tripathi TanyaGospodarska EmiliaGeran RohatSperber Pia SophieSchmitz-Hübsch TanjaPaul FriedemannCarlberg Carsten - MYB is a key transcriptional regulator of hematopoietic cell proliferation, survival, and lineage commitment. Aberrant MYB activity has been linked to hematologic malignancies and clinically relevant features, including poor prognosis and drug resistance. However, the mechanisms by which MYB contributes to drug resistance in leukemia remain unclear. - Source: PubMed
Publication date: 2026/07/18
Fang HuiyingWang YuchengZhou ZhenhuaLi XinyuSun ChangZhang JunfangHan Bingshe - Multidrug resistance (MDR) is a major determinant of relapse-associated mortality in pediatric acute lymphoblastic leukemia (pALL). Although miR-326 downregulation has been associated with poor prognosis, its role in chemoresistance remains undefined. This study investigated the mechanistic contribution of miR-326 to MDR in pALL. - Source: PubMed
Publication date: 2026/06/28
Aberuyi NargesRahgozar SoheilaKatebi Melika - The ATP-binding cassette subfamily A member 2 (ABCA2) gene encodes an ABC transporter protein. Bi-allelic loss-of-function variants in ABCA2 have been associated with an intellectual disability disorder. We aimed to delineate the phenotypic spectrum of individuals with monoallelic (MV) or bi-allelic (BV) variants in the ABCA2 gene. We collected clinical data via questionnaires and literature review. The ABCA2 protein was constructed using homology modeling. Untargeted plasma metabolomics was performed at Metabolon. A docetaxel toxicity cell culture model system was used to study the effects of plasmid-encoded ABCA2 and four ABCA2 variants (p.Asp615Glu [c.1845C>A], p.Phe754Ser [c.2261T>C], p.Ile786del [c.2356_2358del], and p.Arg926Trp [c.2776C>T]) on cell viability. Seventeen individuals with seventeen candidate ABCA2 variants were identified (seven MVs and ten BVs). Protein modeling predicted a likely significant impact for eight of 13 assessed variants. In cell viability assays, enforced expression of wild-type ABCA2 reduced viability in docetaxel-exposed cells. In contrast, none of the four variants affected viability, suggesting a loss or a marked reduction in transporter function. Untargeted metabolomics of three samples from two individuals showed a trend toward lower levels of polyunsaturated acylcarnitines. This study describes 17 individuals with candidate variants in the ABCA2 gene. The cell viability assays revealed that four variants (p.Asp615Glu, p.Phe754Ser, p.Ile786del, and p.Arg926Trp) had an altered ability to function as a transporter compared to wild-type ABCA2. Further studies are needed to clarify the pathomechanism of ABCA2 and the clinical significance of the variants. - Source: PubMed
Publication date: 2026/06/25
Oja Kaisa TReinson KaritIlisson MihkelÖrd DaimaWojcik Monica HSeaby Eleanor GWittmann Bryan MKennedy Adam DDeBalsi KarenZweier ChristianeVasileiou GeorgiaAlkhawaja Issam AWirth ThomasSyrbe SteffenPlatzer KonradAlyamani SuadAlkuraya Fowzan SRos-Pardo DavidMarcos-Alcalde IñigoGómez-Puertas PaulinoVidailhet MarieSu KeFan ShaohuaMa YuWang YiRenieri AlessandraPinto Anna MariaAlmadhoun FarahPetersen Andrea KMagnussen KariBodamer OlafAlanzi TalalMohamed SararAlrabee HadeelAlhaddad BaderBakur KhadijahFleischer NicoleBegtrup AmberÖrd TõnisPajusalu SanderÕunap Katrin - The gut microbiome is a critical regulator of host health, but how it mediates the therapeutic effects of drugs targeting neurodegenerative diseases like diabetic cognitive impairment (DCI) is unclear. Here, we investigated whether the neuroprotective effects of the GLP-1 agonist semaglutide (SE) are linked to its modulation of the gut-brain axis. - Source: PubMed
Publication date: 2026/03/26
Qi LiqinKang HuiminLi XiaofenWang LijingLin YinchenZhan MenglanZeng FeihuiXiao ZhiwenLiu XiaoyingChen ZhouLiu Libin