Three probes were used for the chromosomal assignment of the human SPI1 oncogene: cDb1 and RaB2 correspond respectively to murine Spi1 and human SPI1 cDNA probes; C45a6B probe is a murine genomic DNA sequence located in the Spi1 5' region and is known as a major SFFV integration site in murine erythroleukemia cells.
Moreover, transforming growth factor-β induced RUNX2/ p57 overexpression and specific RUNX2 knockdown supported a role for RUNX2 in epithelial mesenchymal transition, which was demonstrated through loss of function assays in adenocarcinoma A549 lung cancer cell line.
cDNA cloning and sequence analysis of beta ig-h3, a novel gene induced in a human adenocarcinoma cell line after treatment with transforming growth factor-beta.
betaig-h3 (TGFBI, keratoepithelin) was first identified as a transforming growth factor-beta1 (TGF-beta1)-inducible gene in a human lung adenocarcinoma cell line.
Analyzing the mechanism of TGFBI up-regulation in clear cell carcinoma, we identified a novel VHL target, a Kruppel-like transcriptional factor 10 (KLF10).
Three probes were used for the chromosomal assignment of the human SPI1 oncogene: cDb1 and RaB2 correspond respectively to murine Spi1 and human SPI1 cDNA probes; C45a6B probe is a murine genomic DNA sequence located in the Spi1 5' region and is known as a major SFFV integration site in murine erythroleukemia cells.
The resulting gene-sets identified by our CSD analysis also contain many genes that so far have not been recognized as having a role in glioblastoma, but are good candidates for further studies.
beta ig-h3-specific fluorescence was found just beneath detached epithelium in the sub-epithelial matrix, abnormal Descemet's membrane and posterior collagenous layer.
The serine protease high-temperature requirement protein A1 (HtrA1) is associated with protein-misfolding disorders such as Alzheimer's disease and transforming growth factor β-induced protein (TGFBIp)-linked corneal dystrophy.
Two mutations in the TGFBI gene (A546D and P551Q) cosegregated with LCD in an extensively studied family that lacked the R124C mutation that frequently accompanies this form of corneal amyloidosis.
The lattice phenotype resulting from the TGFBIA546D mutation in this family is distinct from that observed in a previously described pedigree carrying the A546D mutation and exhibiting a phenotype designated "polymorphic corneal amyloidosis".
Significantly, these peptides have been previously identified in amyloid deposits <i>in vivo</i>, supporting the idea that HtrA1 is a causative agent for TGFBIp-associated amyloidosis in corneal dystrophy.
The study reveals previously unknown differences between the protein composition of GCD1 and LCD1 aggregates, and confirms the presence of the HtrA1 protease in LCD1-amyloid aggregates.
In contrast with the patient carrying the Gly623Asp mutation of the TGFBI gene described by Afshari et al, our cases presented with Salzmann's nodular degeneration-like clinical features and their specimens contained KE2-positive amyloid.