About: Testin is a research topic. Over the lifetime, 81 publications have been published within this topic receiving 2139 citations. The topic is also known as: TESS & TESS-2.
TL;DR: The coupled pharmacological manipulation of methylation with gene profiling provides a powerful means to identify candidate tumor-suppressor genes for subsequent evaluation and may lead to the identification of genes whose epigenetic dysregulation is integral to glioblastoma tumorigenesis.
Abstract: Glioblastoma, the most aggressive and least treatable form of malignant glioma, is the most common human brain tumor. Although many regions of allelic loss occur in glioblastomas, relatively few tumor suppressor genes have been found mutated at such loci. To address the possibility that epigenetic alterations are an alternative means of glioblastoma gene inactivation, we coupled pharmacological manipulation of methylation with gene profiling to identify potential methylation-regulated, tumor-related genes. Duplicates of three short-term cultured glioblastomas were exposed to 5 microM 5-aza-dC for 96 h followed by cRNA hybridization to an oligonucleotide microarray (Affymetrix U133A). We based candidate gene selection on bioinformatics, reverse transcription-polymerase chain reaction (RT-PCR), bisulfite sequencing, methylation-specific PCR and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Two genes identified in this manner, RUNX3 and Testin (TES), were subsequently shown to harbor frequent tumor-specific epigenetic alterations in primary glioblastomas. This overall approach therefore provides a powerful means to identify candidate tumor-suppressor genes for subsequent evaluation and may lead to the identification of genes whose epigenetic dysregulation is integral to glioblastoma tumorigenesis.
TL;DR: The demonstrated usefulness of testin in examining Sertoli-germ cell interactions is demonstrated, with virtually no testin found in the luminal fluid and cytosols of the testis and epididymis when the intercellular junctions were not previously disrupted, suggesting that secreted testin may be reabsorbed by testicular cells in vivo.
TL;DR: The findings suggest that TESTIN may represent a candidate tumor suppressor gene at 7q31.2, showing loss of heterozygosity in human malignancies and the genomic structure of the human TESTIN locus was determined and three alternative transcripts were characterized.
TL;DR: The fact that TES localises to regions of cell adhesion suggests that it functions in events related to cell motility and adhesion, and it is demonstrated that fibroblasts stably overexpressing TES have an increased ability to spread on fibronectin.
Abstract: Previously, we identified TES as a novel candidate tumour suppressor gene that mapped to human chromosome 7q31.1. In this report we demonstrate that the TES protein is localised at focal adhesions, actin stress fibres and areas of cell-cell contact. TES has three C-terminal LIM domains that appear to be important for focal adhesion targeting. Additionally, the N-terminal region is important for targeting TES to actin stress fibres. Yeast two-hybrid and biochemical analyses yielded interactions with several focal adhesion and/or cytoskeletal proteins including mena, zyxin and talin. The fact that TES localises to regions of cell adhesion suggests that it functions in events related to cell motility and adhesion. In support of this, we demonstrate that fibroblasts stably overexpressing TES have an increased ability to spread on fibronectin.
TL;DR: The distribution of these proteins in biological fluids were compared with those of testibumin and rat androgen binding protein (rABP) and the results suggest that testins are unique testicular proteins that can be used to study Sertoli cell-germ cell interactions in the seminiferous epithelium.