Search results for: VBP1
#37576193 
2023/07/26
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Cuproptosis-related genes prediction feature and immune microenvironment in major depressive disorder.
Major depressive disorder (MDD) is a severe, unpredictable, ill-cured, relapsing neuropsychiatric disorder. A recently identified type of death called cuproptosis has been linked to a number of illnesses. However, the influence of cuproptosis-related genes in MDD has not been comprehensively assessed in prior study.Daoyun Lei, Jie Sun, Jiangyan Xia
2228 related Products with: Cuproptosis-related genes prediction feature and immune microenvironment in major depressive disorder.
2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box5mg50100μg100ug100 50 ug
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#37201586 2023/05/16
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VBP1 negatively regulates CHIP and selectively inhibits the activity of hypoxia-inducible factor (HIF)-1α but not HIF-2α.
Hypoxia-inducible factor-1 (HIF-1) is a critical transcription factor that regulates the expression of genes involved in cellular adaptation to low oxygen levels. Aberrant regulation of the HIF-1 signaling pathway is linked to various human diseases. Previous studies have established that HIF-1α is rapidly degraded in a von Hippel-Lindau protein (pVHL)-dependent manner under normoxic conditions. In this study, we find that pVHL binding protein 1 (VBP1) is a negative regulator of HIF-1α but not HIF-2α using zebrafish as an in vivo model and in vitro cell culture models. Deletion of vbp1 in zebrafish caused Hif-1α accumulation and upregulation of Hif target genes. Moreover, vbp1 was involved in the induction of hematopoietic stem cells (HSCs) under hypoxic conditions. However, VBP1 interacted with and promoted the degradation of HIF-1α in a pVHL-independent manner. Mechanistically, we identify the ubiquitin ligase CHIP and HSP70 as new VBP1 binding partners and demonstrate that VBP1 negatively regulated CHIP and facilitated CHIP-mediated degradation of HIF-1α. In patients with clear cell renal cell carcinoma (ccRCC), lower VBP1 expression was associated with worse survival outcomes. In conclusion, our results link VBP1 with CHIP stability and provide insights into underlying molecular mechanisms of HIF-1α-driven pathological processes.Yiming Yue, Yanfei Tang, Hao Huang, Dongdong Zheng, Cong Liu, Haifeng Zhang, Yunzhang Liu, Yun Li, Xiangrong Sun, Ling Lu
2540 related Products with: VBP1 negatively regulates CHIP and selectively inhibits the activity of hypoxia-inducible factor (HIF)-1α but not HIF-2α.
100ug125 mg100ug15 ml200ul100 mg0.1 mg16 Arrays/Slide10
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#37035734 2023/03/24
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Identification of key pathways, genes and immune cell infiltration in hypoxia of high-altitude acclimatization meta-analysis and integrated bioinformatics analysis.
For individuals acutely exposed to high-altitude regions, environmental hypobaric hypoxia induces several physiological or pathological responses, especially immune dysfunction. Therefore, hypoxia is a potentially life-threatening factor, which has closely related to high-altitude acclimatization. However, its specific molecular mechanism is still unclear. The four expression profiles about hypoxia and high altitude were downloaded from the Gene Expression Omnibus database in this study. Meta-analysis of GEO datasets was performed by NetworkAnalyst online tool. Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene ontology (GO) enrichment analysis, and visualization were performed using R (version 4.1.3) software, respectively. The CIBERSORT analysis was conducted on GSE46480 to examine immune cell infiltration. In addition, we experimentally verified the bioinformatics analysis with qRT-PCR. The meta-analysis identified 358 differentially expressed genes (DEGs), with 209 upregulated and 149 downregulated. DEGs were mostly enriched in biological processes and pathways associated with hypoxia acclimatization at high altitudes, according to both GO and KEGG enrichment analyses. ERH, VBP1, BINP3L, TOMM5, PSMA4, and POLR2K were identified by taking intersections of the DEGs between meta-analysis and GSE46480 and verified by qRT-PCR experiments, which were inextricably linked to hypoxia. Immune infiltration analysis showed significant differences in immune cells between samples at sea level and high altitudes. Identifying the DEGs and pathways will improve our understanding of immune function during high-altitude hypoxia at a molecular level. Targeting hypoxia-sensitive pathways in immune cells is interesting in treating high-altitude sickness. This study provides support for further research on high-altitude acclimatization.Qiong Li, Zhichao Xu, Fujin Fang, Yan Shen, Huan Lei, Xiaobing Shen
1940 related Products with: Identification of key pathways, genes and immune cell infiltration in hypoxia of high-altitude acclimatization meta-analysis and integrated bioinformatics analysis.
2.5 mg1x10e7 cells1 module400 ug24 tests
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#36452459 2022/11/14
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Identification of microRNA editing sites in three subtypes of leukemia.
Leukemia is an aberrant hyper-proliferation of immature blood cells that do not form solid tumors. The transcriptomes of microRNAs (miRNAs) of leukemia have been intensively explored. However, miRNA editing of leukemia has not been extensively studied. To identify miRNA editing patterns and explore their functional relevance in leukemia, we analyzed 200 small RNA sequencing profiles of three subtypes of leukemia and identified hundreds of miRNA editing sites in three subtypes of leukemia. Then, we compared the editing levels of identified miRNA editing sites in leukemia and normal controls. Many miRNAs were differential edited in different subtypes of leukemia. We also found the editing levels of 3'-A editing sites of hsa-mir-21-5p and hsa-mir-155-5p decreased in chronic lymphocytic leukemia patients with radiation treatments. By integrating PAR-CLIP sequencing profiles, we predicted the targets of original and edited miRNAs. One of the edited miRNA, hsa-let-7b_5c, with an additional cytosine at 5' end of hsa-let-7b-5p, potentially targeted VBP1 and CTDSP1. CTDSP1 was significantly downregulated in T-ALL compared to normal controls, which might be originated from the hyperediting of hsa-let-7b-5p in T-ALL. Our study provides a comprehensive view of miRNA editing in three different subtypes of leukemia.Wenping Xie, Jun Yang, Nan Zhou, Hao Ding, Guangchen Zhou, Shuai Wu, Shiyong Guo, Wanran Li, Lei Zhang, Huaide Yang, Chunyi Mao, Yun Zheng
2509 related Products with: Identification of microRNA editing sites in three subtypes of leukemia.
100 ul50 ul 5 G50 ul100 ul1 set (5 x 1 ml)500 samples100 100.00 ug1 mg
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#36090090 2022/08/15
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Interaction network of African swine fever virus structural protein p30 with host proteins.
African swine fever virus (ASFV) is a complex nucleocytoplasmic large DNA virus (NCLDV) that causes a lethal hemorrhagic disease that is currently threatening the global pig industry. ASFV structural protein p30 is a membrane phosphoprotein that suggests it may play a regulatory role, possibly in signal transduction. Despite its significance in internalization into host cells, the interaction between p30 and host proteins is relatively unknown. In this study, we describe the application of a DUALmembrane yeast two-hybrid assay to screen a primary porcine alveolar macrophages cDNA library and analyze the interactome of p30 protein. Our data identify seven host cellular proteins (DAB2, RPSA, OAS1, PARP9, CAPG, ARPC5, and VBP1) that putatively interact with the p30. We further verified the interaction between p30 and host proteins by laser confocal microscopy, co-immunoprecipitation, and GST-pulldown assay. To further understand the relationship between host proteins and p30, we drew the interaction network diagram and analyzed the functional enrichment of each host protein. Enrichment analysis of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes indicated that host proteins were mainly related to endocytosis, actin cytoskeleton regulation, and innate immunity. Collectively, we identified the interaction between p30 and host cell protein using a membrane protein yeast two-hybrid system, which increases our knowledge of the interaction between ASFV and the host and informs future research on antiviral strategies.Xiongnan Chen, Xiaojun Chen, Yifan Liang, Sijia Xu, Zhijun Weng, Qi Gao, Zhao Huang, Guihong Zhang, Lang Gong
1477 related Products with: Interaction network of African swine fever virus structural protein p30 with host proteins.
100100100ug Lyophilized10005001000100ug Lyophilized5005100100ug Lyophilized500
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#34329303 2021/07/30
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Histone deacetylase inhibitor induced pVHL-independent degradation of HIF-1α and hierarchical quality control of pVHL via chaperone system.
The mortality rate of ovarian cancer is increasing and the role of hypoxia inducible factor-1α (HIF-1α) in tumor progression has been confirmed. von Hippel-Lindau tumor suppressor protein (pVHL) binds HIF-1α and mediates proteasome degradation of HIF-1α. Besides, histone deacetylase inhibitor (HDACi) mitigates tumor growth via targeting HIF-1α, whereas underlying mechanism still requires investigation. In this research, we exposed ovarian cancer cell lines OV-90 and SKOV-3 to escalating concentrations of HDACi LBH589. As a result, cell viability was significantly suppressed and expression of HIF-1α was remarkably reduced along with decreased levels of signal molecules, including phosphoinositide 3-kinase (PI3K) and glycogen synthase kinase 3β (GSK3β) (P = 0.000). Interestingly, pVHL was expressed in a notably declining tendency (P = 0.000). Chaperone heat shock protein-70 (HSP70) was expressed in an ascending manner, whereas expression of chaperonin TCP-1α was reduced clearly (P = 0.000). Besides, co-inhibition of pVHL plus HDAC did not contribute to a remarkable difference in HIF-1α expression as compared with single HDAC inhibition. Furthermore, both cell lines were transfected with plasmids of VHL plus VHL binding protein-1 (VBP-1). Consequently, the expression of HIF-1α as well as lactate dehydrogenase-A (LDHA) was remarkably decreased (P = 0.000). These findings indicate HDACi may repress expression of HIF-1α via inhibiting PI3K and GSK3β and promote degradation of HIF-1α via HSP70, independent of pVHL. Additionally, a sophisticated network of HDAC and chaperones may involve in pVHL quality control.Jieming Ni, Anping Ni
2201 related Products with: Histone deacetylase inhibitor induced pVHL-independent degradation of HIF-1α and hierarchical quality control of pVHL via chaperone system.
5mg10mg 5 G50mg10mgN/A 5mg10mg 70 Slides 3 mg50 ug
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#34199727 2021/06/04
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The -Mediated Xq28 Duplication Syndrome: An Intersection between Neurodevelopment, Immunology, and Cancer.
The -mediated Xq28 duplication syndrome is a rare X-linked intellectual disability syndrome (XLIDS) arising from a duplication of the segment between intron 22 homologous regions 1 and 2, on the q28 subregion of the X chromosome. The main clinical features of the syndrome include intellectual disability, neurobehavioral abnormalities, and dysmorphic facial features. Due to the X-linked nature of the syndrome, affected males exhibit more severe phenotypes compared with heterozygous females. A unique distinguishing feature of the syndrome across the sexes, however, is a peculiar combination of recurrent sinopulmonary infections and atopy exclusively seen in a subset of affected males. In addition to the 'typical' 0.5 Mb duplication detected in most cases reported to date with the syndrome, a shortened centromeric version, and another 0.2 Mb telomerically shifted one, have been recently identified, with most detected duplications being maternally inherited, except for three recent cases found to have de novo duplications. Interestingly, a recently reported case of an affected male suggests a possible association of the syndrome with multiple malignancies, an observation that has been recently replicated in two pediatric patients. As a result, a better understanding of the pathogenesis of -mediated Xq28 duplication syndrome may grant us a better understanding of the sex-specific differences in immunological responses, as well as the potential role of the genes involved by the duplication, in oncogenesis.Rami A Ballout, Ayman W El-Hattab
2978 related Products with: The -Mediated Xq28 Duplication Syndrome: An Intersection between Neurodevelopment, Immunology, and Cancer.
100ul 100ul1 kit(96 Wells)1mg 6 ml Ready-to-use 0.1 mg10 mg
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#33137104 2020/11/02
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The prefoldin complex stabilizes the von Hippel-Lindau protein against aggregation and degradation.
Loss of von Hippel-Lindau protein pVHL function promotes VHL diseases, including sporadic and inherited clear cell Renal Cell Carcinoma (ccRCC). Mechanisms controlling pVHL function and regulation, including folding and stability, remain elusive. Here, we have identified the conserved cochaperone prefoldin complex in a screen for pVHL interactors. The prefoldin complex delivers non-native proteins to the chaperonin T-complex-protein-1-ring (TRiC) or Cytosolic Chaperonin containing TCP-1 (CCT) to assist folding of newly synthesized polypeptides. The pVHL-prefoldin interaction was confirmed in human cells and prefoldin knock-down reduced pVHL expression levels. Furthermore, when pVHL was expressed in Schizosaccharomyces pombe, all prefoldin mutants promoted its aggregation. We mapped the interaction of prefoldin with pVHL at the exon2-exon3 junction encoded region. Low levels of the PFDN3 prefoldin subunit were associated with poor survival in ccRCC patients harboring VHL mutations. Our results link the prefoldin complex with pVHL folding and this may impact VHL diseases progression.Franck Chesnel, Anne Couturier, Adrien Alusse, Jean-Philippe Gagné, Guy G Poirier, Dominique Jean, François-Michel Boisvert, Pauline Hascoet, Luc Paillard, Yannick Arlot-Bonnemains, Xavier Le Goff
1747 related Products with: The prefoldin complex stabilizes the von Hippel-Lindau protein against aggregation and degradation.
100 U1mg10250 IU100.00 ul100ul500 Units0.5 ml 100 G
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#32989053 2020/09/28
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VBP1 modulates Wnt/β-catenin signaling by mediating the stability of the transcription factors TCF/LEFs.
The Wnt/β-catenin pathway is one of the major pathways that regulates embryonic development, adult homeostasis, and stem cell self-renewal. In this pathway, transcription factors T-cell factor and lymphoid enhancer factor (TCF/LEF) serve as a key switch to repress or activate Wnt target gene transcription by recruiting repressor molecules or interacting with the β-catenin effector, respectively. It has become evident that the protein stability of the TCF/LEF family members may play a critical role in controlling the activity of the Wnt/β-catenin signaling pathway. However, factors that regulate the stability of TCF/LEFs remain largely unknown. Here, we report that pVHL binding protein 1 (VBP1) regulates the Wnt/β-catenin signaling pathway by controlling the stability of TCF/LEFs. Surprisingly, we found that either overexpression or knockdown of VBP1 decreased Wnt/β-catenin signaling activity in both cultured cells and zebrafish embryos. Mechanistically, VBP1 directly binds to all four TCF/LEF family members and von Hippel-Lindau tumor-suppressor protein (pVHL). Either overexpression or knockdown of VBP1 increases the association between TCF/LEFs and pVHL and then decreases the protein levels of TCF/LEFs via proteasomal degradation. Together, our results provide mechanistic insights into the roles of VBP1 in controlling TCF/LEFs protein stability and regulating Wnt/β-catenin signaling pathway activity.Haifeng Zhang, Xiaozhi Rong, Caixia Wang, Yunzhang Liu, Ling Lu, Yun Li, Chengtian Zhao, Jianfeng Zhou