HOXD11 antibody - middle region (ARP31966_P050)
- Known as:
- HOXD11 (anti-) - middle region (ARP31966_P050)
- Catalog number:
- arp31966_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HOXD11 antibody - middle region (ARP31966_P050)
Related genes to: HOXD11 antibody - middle region (ARP31966_P050)
- Gene:
- HOXD11 NIH gene
- Name:
- homeobox D11
- Previous symbol:
- HOX4, HOX4F
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2015-08-25
Related products to: HOXD11 antibody - middle region (ARP31966_P050)
Related articles to: HOXD11 antibody - middle region (ARP31966_P050)
- Glioma is the most common primary malignant tumor of the central nervous system, characterized by high invasiveness and a high recurrence rate. The clinical therapeutic efficacy remains limited, necessitating the exploration of novel molecular mechanisms and therapeutic targets. Long non-coding RNAs (lncRNAs), as key epigenetic regulators in tumor progression, can influence tumorigenesis and development through lncRNA-miRNA-mRNA regulatory axes. Here, we reveal the critical role of the lncRNA CROCCP2/miR-5584-5p/HOXD11 axis in glioma. LncRNA CROCCP2 was significantly upregulated in glioma tissues and cell lines, in vitro, markedly promoting the proliferation, migration, and invasion of glioma cells. Mechanistically, LncRNACROCCP2 acts as a competing endogenous RNA to sponge miR-5584-5p, thereby relieving its suppression of the target gene HOXD11, leading to HOXD11 upregulation. HOXD11 negatively regulated autophagy, as reflected by reduced LC3B-II and Beclin1 levels and increased p62 expression. Conversely, CROCCP2 or HOXD11 knockdown activated autophagy and provided supportive evidence for ongoing autophagic flux based on the addition of LC3B-II and p62 after bafilomycin A1 treatment. Knockdown of either lncRNA CROCCP2 or HOXD11 suppressed glioma cell proliferation, migration, and invasion in vitro. In addition, HOXD11 silencing markedly inhibited subcutaneous and intracranial tumor growth in nude mice; furthermore, HOXD11 knockout can even halt the growth of subcutaneous tumors. Collectively, our findings suggest that the lncRNA CROCCP2/miR-5584-5p/HOXD11 axis contributes to glioma cell malignant phenotypes in vitro and tumor growth in vivo, at least partly through negative regulation of autophagy, providing a potential molecular target for glioma therapy. - Source: PubMed
Publication date: 2026/06/04
Wang FengLei GanniPeng YuanLiu MaoqiaoJiang TianqiWang MinghuiWang ZhePu JunLiu Jia - Colorectal cancer (CRC) is a prevalent malignancy worldwide, and epigenetic modifications, particularly methylation of key genes, play a crucial role in its initiation and progression. DNA methyltransferase 1 (DNMT1) is aberrantly overexpressed in CRC; however, its specific mechanisms of action and downstream targets remain unclear. This study aims to elucidate how DNMT1 epigenetically regulates HOXD11 expression and subsequently influences CRC progression. - Source: PubMed
Publication date: 2026/05/26
Wang JingXiang RanHe ChunhuaLi FuyeLiu Meng - Prostate cancer resistance to androgen deprivation therapy often involves neuroendocrine transformation. Using single-cell RNA sequencing of transgenic adenocarcinoma of the mouse prostate (TRAMP) mice across pathological stages (early adenocarcinoma to late neuroendocrine prostate cancer [NEPC]), we find an early neuroendocrine-initiating cluster marked by elevated HOXD11, conserved in human NEPC. Genetic suppression of HOXD11 blocks neuroendocrine differentiation and restores androgen receptor (AR) signaling. Mechanistically, HOXD11 directly activates FOXA2 and N-methyl-D-aspartate receptor (NMDAR) subunits (GRIN1/GRIN3A), pathways upregulated in NEPC and linked to poor prognosis. Pharmacological NMDAR inhibition with memantine suppresses NEPC progression preclinically. Notably, a preliminary clinical observation in one evaluable patient with chemotherapy-failed NEPC shows radiographic regression of primary and metastatic lesions after memantine treatment. These findings establish HOXD11 as a driver of neuroendocrine transformation and support further investigation of memantine as a candidate therapeutic strategy for NEPC. - Source: PubMed
Publication date: 2026/05/13
Wu TiangeTan SongMao LikaiZhang RuixinHuang EnyaoWang CanLin HaoWang HuiWang XiaolinChen ShengrongLu HaowenLuo CaichenChen YuruiCheng YifeiXia TianyiYan XiangyuZhu ZiqiYou ZonghaoZhi YunlaiZheng XiejunhaoGao TianShi FanChen ZhanFan CongbinZhong FeiNa RongChen MingTeng Gao-JunZhu YiniLi WenchaoXu Bin - Synovial sarcoma (SyS) is a common type of soft tissue sarcoma, characterized by slow growth, high rates of metastasis, and diverse clinical symptoms. This malignancy is defined by the presence of the SS18-SSX fusion protein and the corresponding SS18-SSX program that promotes the core oncogenic pathways and a wide spectrum of tumor cell phenotypes. In this study, we used single-cell RNA sequencing to explore SyS diversity, highlighting four molecular subtypes. The mesenchymal NKD2 SyS is characterized by the increased BMP signaling in tumor cells and the most severe immune escape and chemoresistance profile. The poorly differentiated HOXD11 SyS displays the highest expression of the core oncogenic program and the likely suppression of the immune response through CXCL and MIF signaling. The fibroblast-like DCN SyS demonstrates high levels of mesenchymal differentiation, a surprising drop in the SS18-SSX program expression, and the angiogenesis-oriented cell-cell interactions. The biphasic EPCAM SyS has the highest levels of differentiation and lowest levels of the core oncogenic program. Our data complements the traditional classification of SyS and suggests that the monophasic mesenchymal SyS might consist of two molecular subtypes. - Source: PubMed
Publication date: 2026/04/15
Toropov Artem LKopantseva Elena EIkonnikov Alexander VMenyailo Maxim EFetisov Timur IStroganova Anna MMeshkova Daria AKozlov Nikolay AShtompel Polina AKhazanova Sofya ATrapeznikova Ekaterina AKirsanov Kirill ITararykova Anastasia AYakubovskaya Marianna GDenisov Evgeny V - Salamanders provide excellent models for studying vertebrate evolution, development, and regeneration. To further advance the newt as a model organism in biology, we conducted draft genome sequencing of 20 Gb of an inbred newt (). As part of this study, the intergenic region is expanded by over 1 Mb owing to the massive insertion of repetitive sequences including newt-specific satellite DNA. Interestingly, and , genes that are typically involved in vertebrate development, are absent in salamanders. Co-option of genes, which encode sex pheromone ligands, suggests a diversification of reproductive behavior among salamanders. Moreover, a limb enhancer of , MFCS1/ZRS, retains its function, even though it is positioned approximately 5 Mb away from the promoter. Furthermore, we have identified a functional -element potentially associated with limb regeneration in this enhancer. The newt genome yields crucial insights into amphibian evolution, behavior, development, and regeneration. - Source: PubMed
Publication date: 2025/09/09
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