Search Results for: tincr

Featured long non-coding RNA - TINCR

lncRNAThe human genome encodes several thousand long non-protein coding transcripts>200 nucleotides in length, a subset of which were shown to play important roles in regulation of gene expression. Researchers at the University of Regensburg, Germany recently identified TINCR, a lncRNA required for induction of key differentiation genes in epidermal tissue, including genes mutated in human skin diseases characterized by disrupted epidermal barrier formation. High-throughput analyses of TINCR RNA- and protein-interactomes revealed TINCR interaction with differentiation mRNAs as well as the Staufen1 protein. TINCR, together with Staufen1, seems to stabilize a subset of mRNAs required for epidermal differentiation. Here, the author discusses the emerging roles of Staufen1 and TINCR in the regulation of mammalian cell differentiation mediated by interaction with target mRNAs. They consider a role for TINCR as an epithelial-specific guide for targeting the Staufen1 protein to specific mRNAs, reflecting the increasing complexity of gene regulatory processes in mammalian cells and tissue.

Kretz M. (2013) TINCR, staufen1, and cellular differentiation. RNA Biol [Epub ahead of print]. [abstract]

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  • Long non-coding RNAs (lncRNAs) longer than 200 nucleotides in length are a newly major class of non-coding RNA which have been identified by
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Control of somatic tissue differentiation by the long non-coding RNA TINCR

Several of the thousands of human long non-coding RNAs (lncRNAs) have been functionally characterized however, potential roles for lncRNAs in somatic tissue differentiation remain poorly understood. Here, a team led by researchers at Stanford University School of Medicine show that a 3.7-kilobase lncRNA, terminal differentiation-induced ncRNA (TINCR), controls human epidermal differentiation by a post-transcriptional mechanism. TINCR is required for high messenger RNA abundance of key differentiation genes, many of which are mutated in human skin diseases, including FLG, LOR, ALOXE3, ALOX12B, ABCA12, CASP14 and ELOVL3. TINCR-deficient epidermis lacked terminal differentiation ultrastructure, including keratohyalin granules and intact lamellar bodies.

Stanford researchers discover master regulator of skin development

skin

The surface of your skin, called the epidermis, is a complex mixture of many different cell types — each with a very specific job. The production, or differentiation, of such a sophisticated tissue requires an immense amount of coordination at the cellular level, and glitches in the process can have disastrous consequences. Now, researchers at the Stanford University School of Medicine have identified a master regulator of this differentiation process.

“Disorders of epidermal differentiation, from skin cancer to eczema, will affect roughly one-half of Americans at some point in their lifetimes,” said Paul Khavari, MD, PhD. “Understanding how this differentiation occurs has enormous implications, not just for the treatment of disease, but also for studies of tissue regeneration and even stem cell science.” Khavari is the Carl J. Herzog Professor and chair of the Department of Dermatology.

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