Max Bielschowsky (1869-1940).
Ontology highlight
ABSTRACT:
SUBMITTER: Stahnisch FW
PROVIDER: S-EPMC4363476 | biostudies-other | 2015 Mar
REPOSITORIES: biostudies-other
Similar Datasets
Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the transcription factor MAX.Human SCLC cell lines waere analyzed for mutations at the MAX locus. Those cell lines that were found mutated in MAX and showed no MAX protein expression were used as a models to restore the expression of MAX transcription factor, and Identify MAX signature on Human SCLC. Human SCLC cell lines were hybridyzed in the following manner according for different conditions (Mock -Ø, MAX, shBRG1, MAX-shBRG1): 3 different biological samples for Mock, 3 different biological samples for MAX, 3 different samples for shBRG1 and 3 replicates of the same sample for MAX-shBRG1.
| S-ECPF-GEOD-48559 | biostudies-other
Project description:Background:Genomic studies have revealed that multiple genes are mutated at varying frequency in endometrial cancer (EC); however, the relevance of many of these mutations is poorly understood. An EC-specific recurrent mutation in the MAX transcription factor p.His28Arg was recently discovered. We sought to assess the functional consequences of this hotspot mutation and determine its association with cancer-relevant phenotypes. Methods:MAX was sequenced in 509 endometrioid ECs, and associations between mutation status and clinicopathologic features were assessed. EC cell lines stably expressing MAXH28R were established and used for functional experiments. DNA binding was examined using electrophoretic mobility shift assays and chromatin immunoprecipitation. Transcriptional profiling was performed with microarrays. Murine flank (six to 11 mice per group) and intraperitoneal tumor models were used for in vivo studies. Vascularity of xenografts was assessed by MECA-32 immunohistochemistry. The paracrine pro-angiogenic nature of MAXH28R-expressing EC cells was tested using microfluidic HUVEC sprouting assays and VEGFA enzyme-linked immunosorbent assays. All statistical tests were two-sided. Results:Twenty-two of 509 tumors harbored mutations in MAX, including 12 tumors with the p.His28Arg mutation. Patients with a MAX mutation had statistically significantly reduced recurrence-free survival (hazard ratio = 4.00, 95% confidence interval = 1.15 to 13.91, P = .03). MAXH28R increased affinity for canonical E-box sequences, and MAXH28R-expressing EC cells dramatically altered transcriptional profiles. MAXH28R-derived xenografts statistically significantly increased vascular area compared with MAXWT and empty vector tumors (P = .003 and P = .008, respectively). MAXH28R-expressing EC cells secreted nearly double the levels of VEGFA compared with MAXWT cells (P = .03, .005, and .005 at 24, 48, and 72 hours, respectively), and conditioned media from MAXH28R cells increased sprouting when applied to HUVECs. Conclusion:These data highlight the importance of MAX mutations in EC and point to increased vascularity as one mechanism contributing to clinical aggressiveness of EC.
| S-EPMC6279289 | biostudies-literature
Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the transcription factor MAX.Human SCLC cell lines waere analyzed for mutations at the MAX locus. Those cell lines that were found mutated in MAX and showed no MAX protein expression were used as a models to restore the expression of MAX transcription factor, and Identify MAX signature on Human SCLC.
2013-12-28 | GSE48559 | GEO
Project description:Interventions: The MAX study is a multi-centre, stratified, randomised, phase II/III study that aims to compare the safety and efficacy of the combination of capecitabine and bevacizumab and the combination of capecitabine, Mitomycin C (MMC) and bevacizumab, with that of capecitabine monotherapy in patients with previously untreated metastatic colorectal cancer. Treatment will continue until disease progression, unless there is unacceptable toxicity or either the patient or physician requests cessation of treatment.
Primary outcome(s): Progression free survival[Measured after 450 patients have completed 1 year of follow-up]
Study Design: Purpose: Treatment; Allocation: Randomised controlled trial; Masking: Open (masking not used);Assignment: Single group;Type of endpoint: Safety/efficacy
| 2451867 | ecrin-mdr-crc
Project description:Conventional crosslinked ChIP was performed on sgCtrl (control guide RNA) and sgMax (guide RNA against Max) transduced preSCs (early stage SCLC line). We find that loss of MAX leads to decreased MAX, MYC and MNT occupancy.
2020-06-06 | GSE146385 | GEO
Project description:BACKGROUND: Clustering the ESTs from a large dataset representing a single species is a convenient starting point for a number of investigations into gene discovery, genome evolution, expression patterns, and alternatively spliced transcripts. Several methods have been developed to accomplish this, the most widely available being UniGene, a public domain collection of gene-oriented clusters for over 45 different species created and maintained by NCBI. The goal is for each cluster to represent a unique gene, but currently it is not known how closely the overall results represent that reality. UniGene's build procedure begins with initial mRNA clusters before joining ESTs. UniGene's results for soybean indicate a significant amount of redundancy among some sequences reported to be unique mRNAs. To establish a valid non-redundant known gene set for Glycine max we applied our algorithm to the clustering of only mRNA sequences. The mRNA dataset was run through the algorithm using two different matching stringencies. The resulting cluster compositions were compared to each other and to UniGene. Clusters exhibiting differences among the three methods were analyzed by 1) nucleotide and amino acid alignment and 2) submitting authors conclusions to determine whether members of a single cluster represented the same gene or not. RESULTS: Of the 12 clusters that were examined closely most contained examples of sequences that did not belong in the same cluster. However, neither the two stringencies of PECT nor UniGene had a significantly greater record of accuracy in placing paralogs into separate clusters. CONCLUSION: Our results reveal that, although each method produces some errors, using multiple stringencies for matching or a sequential hierarchical method of increasing stringencies can provide more reliable results and therefore allow greater confidence in the vast majority of clusters that contain only ESTs and no mRNA sequences.
| S-EPMC1637028 | biostudies-literature
Project description:Cytosine methylation is a base modification that is often used by genomes to store information that is stably inherited through mitotic cell divisions. Most cytosine DNA methylation is stable throughout different cell types or by exposure to different environmental conditions in plant genomes. Here, we profile the epigenomes of ~100 Glycine max lines to explore the extent of natural epigenomic variation. We also use these data to determine the extent to which DNA methylation variants are linked to genetic variations.
2018-05-07 | GSE114074 | GEO
Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the transcription factor MAX.Human SCLC cell lines waere analyzed for mutations at the MAX locus. Those cell lines that were found mutated in MAX and showed no MAX protein expression were used as a models to restore the expression of MAX transcription factor, and Identify MAX signature on Human SCLC. Human SCLC cell lines were hybridyzed in the following manner according for different conditions (Mock -Ø, MAX, shBRG1, MAX-shBRG1): 3 different biological samples for Mock, 3 different biological samples for MAX, 3 different samples for shBRG1 and 3 replicates of the same sample for MAX-shBRG1.
2013-12-28 | E-GEOD-48559 | biostudies-arrayexpress
Project description:The origin of metazoans required the evolution of mechanisms for maintaining differentiated cell types within a multicellular individual, in part through spatially differentiated patterns of gene transcription. The unicellular ancestor of metazoans was presumably capable of regulating gene expression temporally in response to changing environmental conditions, and spatial cell differentiation in metazoans may represent a co-option of preexisting regulatory mechanisms. Myc is a critical regulator of cell growth, proliferation, and death that is found in all metazoans but absent in other multicellular lineages, including fungi and plants. Homologs of Myc and its binding partner, Max, exist in two of the closest living relatives of animals, the choanoflagellate Monosiga brevicollis (Mb) and Capsaspora owczarzaki, a unicellular opisthokont that is closely related to metazoans and choanoflagellates. We find that Myc and Max from M. brevicollis heterodimerize and bind to both canonical and noncanonical E-boxes, the DNA-binding sites through which metazoan Myc proteins act. Moreover, in M. brevicollis, MbMyc protein can be detected in nuclear and flagellar regions. Like metazoan Max proteins, MbMax can form homodimers that bind to E-boxes. However, cross-species dimerization between Mb and human Myc and Max proteins was not observed, suggesting that the binding interface has diverged. Our results reveal that the Myc/Max network arose before the divergence of the choanoflagellate and metazoan lineages. Furthermore, core features of metazoan Myc function, including heterodimerization with Max, binding to E-box sequences in DNA, and localization to the nucleus, predate the origin of metazoans.
| S-EPMC3203627 | biostudies-literature