A novel p16INK4A transcript.

L Mao; A Merlo; G Bedi; G I Shapiro; C D Edwards; B J Rollins; D Sidransky

Home/Archive/PubMed

PubMed · 7541708

A novel p16INK4A transcript.

L Mao·A Merlo·G Bedi·G I Shapiro·C D Edwards·B J Rollins·D Sidransky

View original source ↗Export metadata ↓

Abstract

p16INK4A and p15INK4B were initially identified as potent inhibitors of activated cyclin/cyclin-dependent kinase complexes. These genes were colocalized to chromosome 9p21, and p16 was subsequently found to be mutated in familial melanoma and deleted in a wide variety of sporadic cancers. We recently found that de novo methylation of a 5' CpG island led to transcriptional block of full-length p16 in many neoplasms. However, the presence of a truncated p16 transcript in methylated cell lines led us to investigate the presence of an alternative promoter or initiation site. We have now identified an abundant alternative p16 transcript in both methylated and unmethylated cell lines generated from a novel sequence (exon 1 beta) potentially involved in the complex regulation of these critical cell cycle genes.

Explore related subjects

Base Sequence Carrier Proteins Chromosomes, Human, Pair 9 Cyclin-Dependent Kinase Inhibitor p16 DNA, Neoplasm Exons Gene Amplification Genes, Tumor Suppressor Humans Molecular Sequence Data Neoplasms Polymerase Chain Reaction RNA Sequence Analysis, DNA Transcription, Genetic Tumor Cells, Cultured Journal Article Research Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

L Mao, A Merlo, G Bedi, G I Shapiro, C D Edwards, B J Rollins, D Sidransky. 1995-07-15. A novel p16INK4A transcript.. https://pubmed.ncbi.nlm.nih.gov/7541708/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2016

miR-503-3p promotes epithelial-mesenchymal transition in breast cancer by directly targeting SMAD2 and E-cadherin.

Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of miR-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined. Here, we found that miR-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified miR-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of miR-503-3p in breast cancer cells inhibited expression of epithelial-mesenchymal transition (EMT)-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their mRNA 3' untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for miR-503-3p in induction of breast cancer EMT and suggest that plasma miR-503-3p may be a useful diagnostic biomarker for breast cancer.

Base Sequence↗

PubMed2003

Identification and characterization of Prp45p and Prp46p, essential pre-mRNA splicing factors.

Through exhaustive two-hybrid screens using a budding yeast genomic library, and starting with the splicing factor and DEAH-box RNA helicase Prp22p as bait, we identified yeast Prp45p and Prp46p. We show that as well as interacting in two-hybrid screens, Prp45p and Prp46p interact with each other in vitro. We demonstrate that Prp45p and Prp46p are spliceosome associated throughout the splicing process and both are essential for pre-mRNA splicing. Under nonsplicing conditions they also associate in coprecipitation assays with low levels of the U2, U5, and U6 snRNAs that may indicate their presence in endogenous activated spliceosomes or in a postsplicing snRNP complex.

Base Sequence↗

PubMed1998

Molecular anatomy of a small chromosome in the green alga Chlorella vulgaris.

A contig covering the entire region of Chlorella vulgaris chromosome I (980 kb long), consisting of 33 cosmid clones has been constructed. By cross-hybridization with other chromosomal DNAs, universal structural elements were detected and localized on the contig. They were composed of at least three different elements: short interspersed DNA elements (SINE)-like elements, long interspersed DNA elements (LINE)-like elements and a putative centromere-like element. At least 36 copies of SINE-like elements were distributed over chromosome I with preferential locations on the right half of the chromosome. DNA fragments containing a SINE-like sequence showed a bent or curved DNA nature on polyacrylamide gel electrophoresis. LINE-like elements were clustered at the left terminus of chromosome I where they formed a tandem array of six copies immediately adjacent to the telomeric repeats. A long sequence element localized at a unique region of chromosome I also existed in a single copy on each chromosome and contained a sequence related to the reverse transcriptase domain of retrotransposons. This feature was compared with the reported centromere-associated elements of higher plants. With its comparative simplicity, the organization of Chlorella chromosome I genomic elements may serve as a prototypic experimental system for deciphering the complexity of huge plant chromosomes.

Base Sequence↗