HOXD8 _ HOXD9 _ HOXD10 EMSA Kit
- Known as:
- HOXD8 _ HOXD9 _ HOXD10 EMSA Kit
- Catalog number:
- AY1194
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- HOXD8 _ HOXD9 HOXD10 EMSA Kit
Related genes to: HOXD8 _ HOXD9 _ HOXD10 EMSA Kit
- Gene:
- HOXD8 NIH gene
- Name:
- homeobox D8
- Previous symbol:
- HOX4, HOX4E
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-08-25
- Gene:
- HOXD9 NIH gene
- Name:
- homeobox D9
- Previous symbol:
- HOX4C, HOX4
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-08-25
- Gene:
- HOXD10 NIH gene
- Name:
- homeobox D10
- Previous symbol:
- HOX4, HOX4D
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2019-04-23
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- Glioblastoma is an aggressive cancer that affects the brain. The Homeobox B and D (HOXB/D) family has been linked to tumor progression, but their exact mechanism remains unclear. - Source: PubMed
Publication date: 2025/04/07
Ahmadi MohsenBazrgar MaryamAkhavan SaeedehFathi MohadesehMousavi PegahGhafouri-Fard Soudeh - HOXD10 is a tumor modulator that can either be a tumor-suppressor or a tumor-promoting gene. However, the role of HOXD10 in glioblastoma multiforme (GBM) remains unclear. - Source: PubMed
Publication date: 2021/10/27
Li YanxinMa KeXie QiZhang XianweiZhang XiuleiChen KuiKong LingfeiQian Rongjun - Skeletal muscle tissue demonstrates global hypermethylation with age. However, methylome changes across the time-course of differentiation in aged human muscle derived cells, and larger coverage arrays in aged muscle tissue have not been undertaken. Using 850K DNA methylation arrays we compared the methylomes of young (27 ± 4.4 years) and aged (83 ± 4 years) human skeletal muscle and that of young/aged heterogenous muscle-derived human primary cells (HDMCs) over several time points of differentiation (0, 72 h, 7, 10 days). Aged muscle tissue was hypermethylated compared with young tissue, enriched for; pathways-in-cancer (including; focal adhesion, MAPK signaling, PI3K-Akt-mTOR signaling, p53 signaling, Jak-STAT signaling, TGF-beta and notch signaling), rap1-signaling, axon-guidance and hippo-signalling. Aged cells also demonstrated a hypermethylated profile in pathways; axon-guidance, adherens-junction and calcium-signaling, particularly at later timepoints of myotube formation, corresponding with reduced morphological differentiation and reductions in MyoD/Myogenin gene expression compared with young cells. While young cells showed little alterations in DNA methylation during differentiation, aged cells demonstrated extensive and significantly altered DNA methylation, particularly at 7 days of differentiation and most notably in focal adhesion and PI3K-AKT signalling pathways. While the methylomes were vastly different between muscle tissue and HDMCs, we identified a small number of CpG sites showing a hypermethylated state with age, in both muscle tissue and cells on genes KIF15, DYRK2, FHL2, MRPS33, ABCA17P. Most notably, differential methylation analysis of chromosomal regions identified three locations containing enrichment of 6-8 CpGs in the HOX family of genes altered with age. With HOXD10, HOXD9, HOXD8, HOXA3, HOXC9, HOXB1, HOXB3, HOXC-AS2 and HOXC10 all hypermethylated in aged tissue. In aged cells the same HOX genes (and additionally HOXC-AS3) displayed the most variable methylation at 7 days of differentiation versus young cells, with HOXD8, HOXC9, HOXB1 and HOXC-AS3 hypermethylated and HOXC10 and HOXC-AS2 hypomethylated. We also determined that there was an inverse relationship between DNA methylation and gene expression for HOXB1, HOXA3 and HOXC-AS3. Finally, increased physical activity in young adults was associated with oppositely regulating HOXB1 and HOXA3 methylation compared with age. Overall, we demonstrate that a considerable number of HOX genes are differentially epigenetically regulated in aged human skeletal muscle and HDMCs and increased physical activity may help prevent age-related epigenetic changes in these HOX genes. - Source: PubMed
Publication date: 2020/09/21
Turner D CGorski P PMaasar M FSeaborne R ABaumert PBrown A DKitchen M OErskine R MDos-Remedios IVoisin SEynon NSultanov R IBorisov O VLarin A KSemenova E APopov D VGenerozov E VStewart C EDrust BOwens D JAhmetov I ISharples A P - Retinoic acid (RA) can induce growth arrest and neuronal differentiation of neuroblastoma cells and has been used in clinic for treatment of neuroblastoma. It has been reported that RA induces the expression of several HOXD genes in human neuroblastoma cell lines, but their roles in RA action are largely unknown. The HOXD cluster contains nine genes (HOXD1, HOXD3, HOXD4, and HOXD8-13) that are positioned sequentially from 3' to 5', with HOXD1 at the 3' end and HOXD13 the 5' end. Here we show that all HOXD genes are induced by RA in the human neuroblastoma BE(2)-C cells, with the genes located at the 3' end being activated generally earlier than those positioned more 5' within the cluster. Individual induction of HOXD8, HOXD9, HOXD10 or HOXD12 is sufficient to induce both growth arrest and neuronal differentiation, which is associated with downregulation of cell cycle-promoting genes and upregulation of neuronal differentiation genes. However, induction of other HOXD genes either has no effect (HOXD1) or has partial effects (HOXD3, HOXD4, HOXD11 and HOXD13) on BE(2)-C cell proliferation or differentiation. We further show that knockdown of HOXD8 expression, but not that of HOXD9 expression, significantly inhibits the differentiation-inducing activity of RA. HOXD8 directly activates the transcription of HOXC9, a key effector of RA action in neuroblastoma cells. These findings highlight the distinct functions of HOXD genes in RA induction of neuroblastoma cell differentiation. - Source: PubMed
Publication date: 2012/08/07
Zha YunhongDing EmilyYang LiqunMao LingWang XiangweiMcCarthy Brian AHuang ShuangDing Han-Fei - HOX genes encode transcription factors, which play a key role in morphogenesis and cell differentiation during embryogenesis. Several observations indicate that a deregulated expression of these genes may result in tumor development and progression. Actually, several HOX genes are aberrantly expressed in many tumors and cell lines derived from them. Little is known about the expression of HOX genes in brain tumors. In the present work, we study the relative expression of HOX-D genes (D1, D3, D4, D8, D9, D10, D11, D12, D13) with real-time polymerase chain reaction in a group of 14 pediatric low-grade gliomas. We compare the HOX-D expression level of the 14 tumors with the average expression level of six non-neoplastic human brain tissues. HOX-D1 and HOX-D12 resulted over-expressed in neoplastic samples with respect to non-neoplastic brain parenchyma. Conversely, HOX-D3 was expressed at a lower level in gliomas with respect to non-neoplastic brain. HOX-D4, HOX-D11, and HOX-D13 were never expressed. HOX-D8, HOX-D9, and HOX-D10 were exceptionally expressed in non-neoplastic samples and irregularly expressed in tumors. The observation that all but three HOX-D genes studied are expressed with different pattern in neoplastic and non-neoplastic brain tissue may support the hypothesis that HOX-D genes play a role in the pathogenesis of pediatric low-grade gliomas. - Source: PubMed
Publication date: 2008/04/11
Buccoliero Anna MariaCastiglione FrancescaRossi Degl'Innocenti DuccioAmmanati FrancoGiordano FlavioSanzo MassimilianoMussa FedericoGenitori LorenzoTaddei Gian Luigi