ANKRD33B
- Known as:
- ANKRD33B
- Catalog number:
- 001633A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANKRD33B
Related genes to: ANKRD33B
- Gene:
- ANKRD33B NIH gene
- Name:
- ankyrin repeat domain 33B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-10-29
- Date modifiied:
- 2016-10-18
Related products to: ANKRD33B
Related articles to: ANKRD33B
- The biological functions and mechanisms of many cell type-specific transcriptional cofactors remain unclear. We previously identified () as a repressive transcriptional cofactor that suppresses Crx-mediated transactivation of photoreceptor genes; however, the biological function of remains unclarified. Here, we investigated the functions of and its paralog, (), in mice of either sex. Single knock-out (KO) mouse retinas of or did not show significant alterations at both histological and functional levels compared with those of control mice. We then established and examined and double knock-out ( DKO) mice. DKO mice exhibited decreased light-evoked activities detected by electroretinogram (ERG), impaired cone photoreceptor morphology revealed by immunohistochemistry, and structural deformity of cone outer segments and synaptic terminals indicated by transmission electron microscopy, followed by cone death at a later stage. Lipidomics analysis revealed elevated ganglioside levels in DKO retinas, consistent with the increased immunoreactivity of GT1b and GD3 in the outer segment layer. RNA-seq analysis was conducted in a cone-enriched context resulting from deficiency and showed that the gene, whose mutations in humans cause retinitis pigmentosa (RP26), was upregulated in triple KO mice. Transcriptional assays showed that PPL suppressed Crx-mediated transactivation of In addition, AAV-mediated overexpression in the mouse retina induced significant photoreceptor cell death. Taken together, these findings suggest that the repressive Panky and Panky-like cofactors, which modulate Crx transcriptional activities and thus ganglioside levels in the mouse retina, are essential for cone photoreceptor structure and maintenance. - Source: PubMed
Publication date: 2026/08/19
Tu Hung-YaGyoten DaichiSumihiro HitoshiMichikawa KayokoMiyanohara YukiHuang ShangyuanAbe ShinyaFujieda KazukiKajimura NaokoChaya TaroIkeda KazutakaFurukawa Takahisa - Glioblastoma (GBM) is an aggressive tumor with limited therapeutic options. Zika virus (ZIKV) has demonstrated activity against GBM; however, the cellular pathways behind this interaction remain unclear. We systematically reviewed open-access primary studies assessing differentially expressed genes (DEGs) in GBM models infected with wild-type or engineered ZIKV using transcriptomic approaches (inclusion criteria); reviews, restricted-access studies, commentaries, preprints, abstracts, and articles lacking data or not meeting these conditions were excluded (PROSPERO CRD420251077092). We performed a pathway analysis of reported DEGs. PubMed and Google Scholar were searched up to 5 March 2025; 139 records were identified and 5 met the eligibility criteria. Risk of bias was evaluated using an adapted ToxRTool for in vitro experiments and the SYRCLE RoB tool for in vivo models. Altogether, 4360 genes were reported as upregulated and 2072 as downregulated; 12 genes (, , , , , , , , , , , and ) were consistently upregulated, none were consistently downregulated. Pathway analysis of the studies providing complete DEG lists identified 23 commonly enriched pathways mostly related to interferon signaling. These findings may help guide future research in this field; nevertheless, methodological heterogeneity limits comparability, reinforcing the need for standardized protocols. Funding: ITpS, CNPq, and FAPEMIG. - Source: PubMed
Publication date: 2026/02/15
Menezes DiegoReis Clarisse RezendeMamede IzabelaGeddes Victor Emmanuel Vianade Souza Renan PedraAguiar Renato Santana - Venezuelan equine encephalitis virus (VEEV) causes encephalitis in humans and equids, and there are no vaccines or therapeutics available for humans. In recent years, non-coding RNAs have emerged as critical regulatory factors affecting different cellular pathways. Specifically, long non-coding RNAs (lncRNAs) have been identified as regulators of antiviral pathways during various viral infections; however, their role in regulating VEEV infection has not been assessed. Here we show differential expression of several lncRNAs in primary mouse target cells infected with a vaccine strain of VEEV (TC-83) but not a pathogenic strain (TrD). Among the differentially expressed genes (DEGs), suppressing lncRNA small nucleolar RNA host gene 15 (Snhg15) resulted in about a 7-fold increase in VEEV TC-83 replication in primary mouse astrocytes. Knockdown of Snhg15 during VEEV TC-83 infection resulted in the suppression of ten genes including Irf1, Junb, Atf3, Relb, Pim1, Hbegf, Ccl5, Ankrd33b, and H2-K2, all of which were also increased during TC-83 infection when the expression of Snhg15 increased in primary mouse astrocytes. Most of these genes are involved in antiviral responses. KEGG pathway analysis confirmed the suppression of both pattern recognition receptor and inflammatory pathways after in Snhg15 knockdown. These data are the first to identify lncRNA responses in encephalitic alphavirus infection and demonstrate important roles for these overlooked RNAs on VEEV infection. - Source: PubMed
Publication date: 2025/05/12
Behnia MahgolYe ChunyanSomfleth KimOyebamiji Olufunmilola MBrayer Kathryn JGuo YanNess Scott ASavan RamBradfute Steven B - Glycaemic traits such as high fasting glucose levels and insulin resistance are positively associated with the risk of type 2 diabetes and other cardiometabolic diseases. Genetic association studies have identified hundreds of associations for each glycaemic trait, yet very few studies have involved continental African populations. We report the results of genome-wide association studies (GWASs) in a pan-African cohort for four glycaemic traits, namely fasting glucose, fasting insulin, insulin resistance (HOMA-IR) and beta cell function (HOMA-B), which are quantitative variables that affect the risk of developing type 2 diabetes. - Source: PubMed
Publication date: 2025/03/01
Chebii Vivien JWade Alisha NCrowther Nigel JNonterah Engelbert AAgongo GodfredSimayi ZBoua Palwende RKisiangani IsaacRamsay MichèleChoudhury AnanyoSengupta Dhriti - : Colorectal cancer (CRC) displays a complex pattern of inheritance. It is postulated that much of the missing heritability of CRC is enriched in high-impact rare alleles, which might play a crucial role in the etiology and susceptibility of CRC. : In this study, an exome-wide association analysis was performed in 146 patients with high-risk CRC in the Middle East and 1395 healthy controls. The aim was to identify rare germline variants in coding regions and their splicing sites associated with high-risk CRC in the Middle Eastern population. : Rare inactivating variants (RIVs) in had the strongest association with high-risk CRC (6/146 in cases vs. 1/1395 in controls, OR = 59.7, = 5.13 × 10), whereas RIVs in , an RAS superfamily member, were significantly associated with high-risk CRC (5/146 case vs. 2/1395 controls, OR = 24.7, = 2.03 × 10). Rare damaging variants in 17 genes were associated with high-risk CRC at the exome-wide threshold ( < 2.5 × 10). Based on the sequence kernel association test, nonsynonymous variants in six genes (, , , , , and ) had a significant association with high-risk CRC. RIVs in -the most common high-penetrance genetic factor-were associated with patients with high-risk CRC in the Middle East. Individuals who inherited RIVs had an approximate 60-fold increased risk of developing CRC and were likely to develop the disease earlier. : We identified new potential CRC predisposition variants in other genes that could play a role in CRC inheritance. However, large collaborative studies are needed to confirm the association of these variants with high-risk CRC. These results provide information for counseling patients with high-risk CRC and their families in our population. - Source: PubMed
Publication date: 2024/11/04
Siraj Abdul KhalidBu RongAzam SaudQadri ZeeshanIqbal KaleemParvathareddy Sandeep KumarAl-Dayel FouadAl-Kuraya Khawla S