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Search results for: YAF2

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#32950105   2020/09/05 To Up

TV-circRGPD6 Nanoparticle Suppresses Breast Cancer Stem Cell-Mediated Metastasis via the miR-26b/YAF2 Axis.

Metastatic tumor is a major contributor to death caused by breast cancer. However, effective and targeted therapy for metastatic breast cancer remains to be developed. Initially, we exploited a feasible biological rationale of the association between metastatic status and tumor-initiating properties in metastatic breast cancer stem cells (BCSCs). Further, we explored that circular RNA RANBP2-like and GRIP domain-containing protein 6 (circRGPD6) regulates the maintenance of stem cell-like characteristics of BCSCs. Targeted expression of circRGPD6 via human telomerase reverse transcriptase (hTERT) promoter-driven VP16-GAL4-woodchuck hepatitis virus post-transcriptional regulatory element (WPRE)-integrated systemic amplifier delivery composite vector (TV-circRGPD6) significantly inhibited expression of stem-cell marker CD44 and increased expression of the DNA damage marker p-H2AX. Furthermore, we determined TV-circRGPD6, alone or synergized with docetaxel, displays significant therapeutic responses on metastatic BCSCs. Mechanistic analyses exploited that TV-circRGPD6 suppresses BCSC-mediated metastasis via the microRNA (miR)-26b/YAF2 axis. Clinically, for the first time, we observed that expressions of circRGPD6 and YAF2 predict a favorable prognosis in patients with breast cancer, whereas expression of miR-26b is an unfavorable prognostic factor. Overall, we have developed a TV-circRGPD6 nanoparticle that selectively expresses circRGPD6 in metastatic BCSCs to eradicate breast cancer metastasis, therefore providing a novel avenue to treat breast cancers.
Xiaoti Lin, Weiyu Chen, Fengqin Wei, Xiaoming Xie

2173 related Products with: TV-circRGPD6 Nanoparticle Suppresses Breast Cancer Stem Cell-Mediated Metastasis via the miR-26b/YAF2 Axis.

One Vial: 5 X 10^6 Cells5 Modulators100ul1 kit

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#32203418   2020/03/23 To Up

RYBP/YAF2-PRC1 complexes and histone H1-dependent chromatin compaction mediate propagation of H2AK119ub1 during cell division.

Stable propagation of epigenetic information is important for maintaining cell identity in multicellular organisms. However, it remains largely unknown how mono-ubiquitinated histone H2A on lysine 119 (H2AK119ub1) is established and stably propagated during cell division. In this study, we found that the proteins RYBP and YAF2 each specifically bind H2AK119ub1 to recruit the RYBP-PRC1 or YAF2-PRC1 complex to catalyse the ubiquitination of H2A on neighbouring nucleosomes through a positive-feedback model. Additionally, we demonstrated that histone H1-compacted chromatin enhances the distal propagation of H2AK119ub1, thereby reinforcing the inheritance of H2AK119ub1 during cell division. Moreover, we showed that either disruption of RYBP/YAF2-PRC1 activity or impairment of histone H1-dependent chromatin compaction resulted in a significant defect of the maintenance of H2AK119ub1. Therefore, our results suggest that histone H1-dependent chromatin compaction plays a critical role in the stable propagation of H2AK119ub1 by RYBP/YAF2-PRC1 during cell division.
Jicheng Zhao, Min Wang, Luyuan Chang, Juan Yu, Aoqun Song, Cuifang Liu, Wenjun Huang, Tiantian Zhang, Xudong Wu, Xiaohua Shen, Bing Zhu, Guohong Li

2884 related Products with: RYBP/YAF2-PRC1 complexes and histone H1-dependent chromatin compaction mediate propagation of H2AK119ub1 during cell division.

100ug96 samples100ug Lyophilized500 MG1.00 flask5 x 1 ml10 ml1 mg100 ug

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#30915747   // To Up

miR-34b inhibits the migration/invasion and promotes apoptosis of non-small-cell lung cancer cells by YAF2.

Lung cancer is the leading cause of cancer death in the world and microRNAs (miRNA) have been found to be involved in the initiation and development of cancer by acting as potential oncogenes or tumor suppressor genes.
X-F Zhuang, L-X Zhao, S-P Guo, S Wei, J-F Zhai, Q-H Zhou

2505 related Products with: miR-34b inhibits the migration/invasion and promotes apoptosis of non-small-cell lung cancer cells by YAF2.

1.00 flask

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#30672021   2019/01/22 To Up

A LINC00341-mediated regulatory pathway supports chondrocyte survival and may prevent osteoarthritis progression.

Osteoarthritis (OA) is the most common degenerative joint disease and results from progressive loss and destruction of articular cartilage and the underlying bone. The disease affects millions of people worldwide with an associated risk of mobility disability. However, the molecular basis underlying OA initiation and progression is not well understood and, currently, there is no effective intervention available to decelerate disease progression or restore degraded cartilage. We have found that lncRNA long intergenic nonprotein coding RNA 341 (LINC00341) is aberrantly downregulated in OA patient tissues and cultured OA chondrocytes. This is likely responsible for the increased apoptosis of chondrocytes and pathological destruction of cartilage. Further investigation has revealed that LINC00341 interacts with miR-141 to suppress its functional binding to the 3'-untranslated region of YY1-associated factor 2 (YAF2) messenger RNA. Aberrant downregulation of LINC00341 thus may ultimately lead to inhibition of the YAF2 protein, which has been implicated to be an antiapoptotic factor. Our study has revealed a new noncoding RNA-mediated regulatory network that highly likely protects chondrocytes by preventing apoptosis under normal conditions. The results will help further explore the molecular details pertaining to the progression of OA and stimulate efforts to develop effective therapies.
Qining Yang, Xiaofei Li, Yongwei Zhou, Weicong Fu, Jinhua Wang, Qiang Wei

2079 related Products with: A LINC00341-mediated regulatory pathway supports chondrocyte survival and may prevent osteoarthritis progression.

25 mg2 Pieces/Box20 100ug96T2.5 mg100ug1 ml50 mg2 Pieces/Box

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#30506950   2018/12/02 To Up

MicroRNA-543 promotes ovariectomy-induced osteoporosis through inhibition of AKT/p38 MAPK signaling pathway by targeting YAF2.

The present study aimed to determine the roles of miRNA-543 in osteoporosis in rats induced by ovariectomy. The osteoporosis rat model was established by ovariectomy induction. MiRNA-543 expression in osteoblasts was measured by quantitative real-time polymerase chain reaction. The cell proliferation and apoptosis were measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry assays, respectively. Western blot analysis was conducted to examine the expression of YAF-2 and AKT signaling. TargetScan analysis and dual-luciferase reporter assay were performed to determine the target gene of miRNA-543. MiRNA-543 was significantly upregulated in osteoporosis rat model. Overexpression of miRNA-543 significantly suppressed cell growth and promoted apoptosis in osteoblasts, whereas downregulation of miRNA-543 significantly enhanced cell growth and inhibited apoptosis. MiRNA-543 upregulation significantly inhibited YAF-2 expression and suppressed the phosphorylation and expression of AKT and p38 mitogen-activated protein kinases (MAPK) in osteoblasts. Furthermore, YAF-2 knockdown enhanced the effects of miRNA-543 on apoptosis in osteoblasts. AKT inhibitor MK2206 and p38 MAPK inhibitor SB203580 also enhanced the effects of miRNA-543 on apoptosis in osteoblasts. Our findings revealed that inhibition of miRNA-543 could protect osteoblasts against ovariectomy-induced osteoporosis through AKT/p38 MAPK signaling pathway by targeting YAF2.
Xiang Li, Lei Ning, Xiangde Zhao, Shuanglin Wan

2674 related Products with: MicroRNA-543 promotes ovariectomy-induced osteoporosis through inhibition of AKT/p38 MAPK signaling pathway by targeting YAF2.

2 Pieces/Box11 inhibitors100ug Lyophilized100ug2 Pieces/Box100ug100ug Lyophilized100ug100 ulInhibitors2 Pieces/Box2 Pieces/Box

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#29959227   2018/06/29 To Up

The polycomb group protein Yaf2 regulates the pluripotency of embryonic stem cells in a phosphorylation-dependent manner.

The polycomb group (PcG) proteins are key epigenetic regulators in stem cell maintenance. PcG proteins have been thought to act through one of two polycomb repressive complexes (PRCs), but more recent biochemical analyses have challenged this model in the identification of noncanonical PRC1 (nc-PRC1) complexes characterized by the presence of Rybp or Yaf2 in place of the canonical Chromobox proteins. However, the biological significance of these nc-PRC1s and the potential mechanisms by which they mediate gene repression are largely unknown. Here, we explore the functional consequences of Yaf2 disruption on stem cell regulation. We show that deletion of Yaf2 results in compromised proliferation and abnormal differentiation of mouse embryonic stem cells (mESCs). Genome-wide profiling indicates Yaf2 functions primarily as a transcriptional repressor, particularly impacting genes associated with ectoderm cell fate in a manner distinct from Rybp. We confirm that Yaf2 assembles into a noncanonical PRC complex, with deletion analysis identifying the region encompassing amino acid residues 102-150 as required for this assembly. Furthermore, we identified serine 166 as a Yaf2 phosphorylation site, and we demonstrate that mutation of this site to alanine (S166A) compromises Ring1B-mediated H2A monoubiquitination and in turn its ability to repress target gene expression. We therefore propose that Yaf2 and its phosphorylation status serve as dual regulators to maintain the pluripotent state in mESCs.
Wukui Zhao, Mengjie Liu, Haijing Ji, Yaru Zhu, Congcong Wang, Yikai Huang, Xiaoqi Ma, Guangdong Xing, Yin Xia, Qing Jiang, Jinzhong Qin

1985 related Products with: The polycomb group protein Yaf2 regulates the pluripotency of embryonic stem cells in a phosphorylation-dependent manner.

2 Pieces/Box100ug2 Pieces/Box100ug1

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#27705745   2016/10/05 To Up

RYBP stimulates PRC1 to shape chromatin-based communication between Polycomb repressive complexes.

Polycomb group (PcG) proteins function as chromatin-based transcriptional repressors that are essential for normal gene regulation during development. However, how these systems function to achieve transcriptional regulation remains very poorly understood. Here, we discover that the histone H2AK119 E3 ubiquitin ligase activity of Polycomb repressive complex 1 (PRC1) is defined by the composition of its catalytic subunits and is highly regulated by RYBP/YAF2-dependent stimulation. In mouse embryonic stem cells, RYBP plays a central role in shaping H2AK119 mono-ubiquitylation at PcG targets and underpins an activity-based communication between PRC1 and Polycomb repressive complex 2 (PRC2) which is required for normal histone H3 lysine 27 trimethylation (H3K27me3). Without normal histone modification-dependent communication between PRC1 and PRC2, repressive Polycomb chromatin domains can erode, rendering target genes susceptible to inappropriate gene expression signals. This suggests that activity-based communication and histone modification-dependent thresholds create a localized form of epigenetic memory required for normal PcG chromatin domain function in gene regulation.
Nathan R Rose, Hamish W King, Neil P Blackledge, Nadezda A Fursova, Katherine Ji Ember, Roman Fischer, Benedikt M Kessler, Robert J Klose

1577 related Products with: RYBP stimulates PRC1 to shape chromatin-based communication between Polycomb repressive complexes.

100 g1 kit(96 Wells)96/kit1 mg 1 G1 ml100ug Lyophilized1 module 25 G100 extractions 1000 ml

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#27136092   2016/05/02 To Up

Loss of Pcgf5 Affects Global H2A Monoubiquitination but Not the Function of Hematopoietic Stem and Progenitor Cells.

Polycomb-group RING finger proteins (Pcgf1-Pcgf6) are components of Polycomb repressive complex 1 (PRC1)-related complexes that catalyze monoubiquitination of histone H2A at lysine 119 (H2AK119ub1), an epigenetic mark associated with repression of genes. Pcgf5 has been characterized as a component of PRC1.5, one of the non-canonical PRC1, consisting of Ring1a/b, Rybp/Yaf2 and Auts2. However, the biological functions of Pcgf5 have not yet been identified. Here we analyzed the impact of the deletion of Pcgf5 specifically in hematopoietic stem and progenitor cells (HSPCs). Pcgf5 is expressed preferentially in hematopoietic stem cells (HSCs) and multipotent progenitors (MPPs) compared with committed myeloid progenitors and differentiated cells. We transplanted bone marrow (BM) cells from Rosa::Cre-ERT control and Cre-ERT;Pcgf5fl/fl mice into lethally irradiated recipient mice. At 4 weeks post-transplantation, we deleted Pcgf5 by injecting tamoxifen, however, no obvious changes in hematopoiesis were detected including the number of HSPCs during a long-term observation period following the deletion. Competitive BM repopulating assays revealed normal repopulating capacity of Pcgf5-deficient HSCs. Nevertheless, Pcgf5-deficient HSPCs showed a significant reduction in H2AK119ub1 levels compared with the control. ChIP-sequence analysis confirmed the reduction in H2AK119ub1 levels, but revealed no significant association of changes in H2AK119ub1 levels with gene expression levels. Our findings demonstrate that Pcgf5-containing PRC1 functions as a histone modifier in vivo, but its role in HSPCs is limited and can be compensated by other PRC1-related complexes in HSPCs.
Sha Si, Yaeko Nakajima-Takagi, Kazumasa Aoyama, Motohiko Oshima, Atsunori Saraya, Hiroki Sugishita, Manabu Nakayama, Tomoyuki Ishikura, Haruhiko Koseki, Atsushi Iwama

1693 related Products with: Loss of Pcgf5 Affects Global H2A Monoubiquitination but Not the Function of Hematopoietic Stem and Progenitor Cells.

5 G1 mg1 x 10^6 cells/vial1 mg1.5 x 10^6 cells10 ug100 µg10.1ml (1mg/ml)125 mg5 x 10A5 cells/vial

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#26775586   2016/01/08 To Up

Cellular functions of programmed cell death 5.

Programmed cell death 5 (PDCD5) was originally identified as an apoptosis-accelerating protein that is widely expressed and has been well conserved during the process of evolution. PDCD5 has complex biological functions, including programmed cell death and immune regulation. It can accelerate apoptosis in different type of cells in response to different stimuli. During this process, PDCD5 rapidly translocates from the cytoplasm to the nucleus. PDCD5 regulates the activities of TIP60, HDAC3, MDM2 and TP53 transcription factors. These proteins form part of a signaling network that is disrupted in most, if not all, cancer cells. Recent evidence suggests that PDCD5 participates in immune regulation by promoting regulatory T cell function via the PDCD5-TIP60-FOXP3 pathway. The stability and expression of PDCD5 are finely regulated by other molecules, such as NF-κB p65, OTUD5, YAF2 and DNAJB1. PDCD5 is phosphorylated by CK2 at Ser119, which is required for nuclear translocation in response to genotoxic stress. In this review, we describe what is known about PDCD5 and its cellular functions.
Ge Li, Dalong Ma, Yingyu Chen

1424 related Products with: Cellular functions of programmed cell death 5.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100tests100ug Lyophilized

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