C12orf34 Over-expression Lysate Product
- Known as:
- C12orf34 Over-expression Lysate Product
- Catalog number:
- GWB-8E6083
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- C12orf34 Over-expression Lysate Product
Ask about this productRelated genes to: C12orf34 Over-expression Lysate Product
- Gene:
- FAM222A NIH gene
- Name:
- family with sequence similarity 222 member A
- Previous symbol:
- C12orf34
- Synonyms:
- FLJ14721
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-20
- Date modifiied:
- 2016-09-30
Related products to: C12orf34 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: C12orf34 Over-expression Lysate Product
- Rat offspring who are exposed to an amorphous formula of curcumin (CUR) from the embryonic stage have anti-anxiety-like behaviors, enhanced fear extinction learning, and increased synaptic plasticity in the hippocampal dentate gyrus (DG). In the present study, we investigated the links between genes with altered methylation status in the neurogenic niche and enhanced neural functions after CUR exposure. We conducted methylation and RNA sequencing analyses of the DG of CUR-exposed rat offspring on day 77 after delivery. Methylation status and transcript levels of candidate genes were validated using methylation-sensitive high-resolution melting and real-time reverse-transcription PCR, respectively. In the CUR group, we confirmed the hypermethylation and downregulation of Gpr150, Mmp23, Rprml, and Pcdh8 as well as the hypomethylation and upregulation of Ppm1j, Fam222a, and Opn3. Immunohistochemically, reprimo-like hilar cells and protocadherin-8 granule cells were decreased and opsin-3 hilar cells were increased by CUR exposure. Both reprimo-like and opsin-3 were partially expressed on subpopulations of glutamic acid decarboxylase 67 γ-aminobutyric acid-ergic interneurons. Furthermore, the transcript levels of genes involved in protocadherin-8-mediated N-cadherin endocytosis were altered with CUR exposure; this was accompanied by Ctnnb1 and Syp upregulation and Mapk14, Map2k3, and Grip1 downregulation, suggesting that CUR-induced enhanced synaptic plasticity is associated with cell adhesion. Together, our results indicate that functionally different genes have altered methylation and expression in different neuronal populations of the hippocampal neurogenic niche, thus enhancing synaptic plasticity after CUR exposure. - Source: PubMed
Publication date: 2024/03/13
Tang QianOjiro RyotaOzawa ShunsukeZou XinyuNakahara JuntaNakao TomohiroKoyanagi MihokoJin MeilanYoshida ToshinoriShibutani Makoto - BETs (bromodomain and extraterminal domain-containing epigenetic reader proteins), including BRD4 (bromodomain-containing protein 4), orchestrate transcriptional programs induced by pathogenic stimuli, as intensively studied in cardiovascular disease and elsewhere. In endothelial cells (ECs), BRD4 directs induced proinflammatory, proatherosclerotic transcriptional responses; BET inhibitors, like JQ1, repress these effects and decrease atherosclerosis. While BET effects in pathogenic conditions have prompted therapeutic BET inhibitor development, BET action under basal conditions, including ECs, has remained understudied. To understand BET action in basal endothelial transcriptional programs, we first analyzed EC RNA-Seq data in the absence versus presence of JQ1 before using BET regulation to identify novel determinants of EC biology and function. - Source: PubMed
Publication date: 2023/11/09
Tzani AspasiaHaemmig StefanCheng Henry SPérez-Cremades DanielHeuschkel Marina AugustoJamaiyar AnuragSingh Sasha AAikawa MasanoriYu Paul BWang TianxiSun YeFeinberg Mark WPlutzky Jorge - The complex nature of Alzheimer's disease (AD) makes it difficult to understand the exact molecular processes leading to neuron death. However, two molecular factors - the production of amyloid-beta plaques and tau tangles - are considered to be linked to AD. A genetic marker for brain atrophy, FAM222A, has been identified by the unique cross-phenotype meta-analysis of genetics imaging and the molecular features show an interaction between the protein aggregatin encoded by FAM222A and amyloid beta (Aβ)-peptide (1-42) via its N-terminal Aβ binding domain, thus increasing Aβ aggregation. Function of Aggregatin protein is unclear, and its 3D structure has not been investigated in experimental analysis, so far. Hence, in the present study, first time in literature, 3D models of FAM222A-encoded Aggregatin were systematically constructed by applying diverse homology modeling approaches and they were used as target structures at the virtual screening of FDA-approved drugs and drugs currently under research in clinical trials. Then, the identified hit molecules were chosen for further molecular dynamics (MD) simulations and post-MD analyses. Our integrated ligand-based and protein-driven-based virtual screening results show that Cefpiramide, Diniprofylline, Fostriecin, and Droperidol may target Aggregatin. - Source: PubMed
Publication date: 2023/07/26
Alabdulraheem Zeyad Tareq JasimDurdagi Serdar - Alzheimer's disease (AD) is the most common form of dementia in the elderly marked by central nervous system (CNS) neuronal loss and amyloid plaques. FAM222A, encoding an amyloid plaque core protein, is an AD brain atrophy susceptibility gene that mediates amyloid-β aggregation. However, the expression interplay between FAM222A and other AD-related pathway genes is unclear. - Source: PubMed
Liang JingjingLaFleur BonnieHussainy SadiyaPerry George - - Source: PubMed
Publication date: 2022/07/11
Yan TingxiangLiang JingjingGao JuWang LuwenFujioka Hisashi Zhu XiaofengWang Xinglong