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Abstract Here we present the Transcription Factor Encyclopedia (TFe), a new web-based compendium of mini review articles on transcription factors (TFs) that is founded on the principles of open access and collaboration. Our consortium of over 100 researchers has collectively contributed over 130 mini review articles on pertinent human, mouse and rat TFs. Notable features of the TFe website include a high-quality PDF generator and web API for programmatic data retrieval. TFe aims to rapidly educate scientists about the TFs they encounter through the delivery of succinct summaries written and vetted by experts in the field. TFe is available at http://www.cisreg.ca/tfe.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2007.01.001 Byline: Branden R. Nelson (a), Byron H. Hartman (a), Sean A. Georgi (b), Michael S. Lan (c), Thomas A. Reh (a)(b) Keywords: Notch activity; Hes1; Hes5; Proneural bHLH transcription factor; Progenitor cell; Neural differentiation; Insulinoma-associated 1 Abstract: In the developing nervous system, the balance between proliferation and differentiation is critical to generate the appropriate numbers and types of neurons and glia. Notch signaling maintains the progenitor pool throughout this process. While many components of the Notch pathway have been identified, the downstream molecular events leading to neural differentiation are not well understood. We have taken advantage of a small molecule inhibitor, DAPT, to block Notch activity in retinal progenitor cells, and analyzed the resulting molecular and cellular changes over time. DAPT treatment causes a massive, coordinated differentiation of progenitors that produces cell types appropriate for their developmental stage. Transient exposure of retina to DAPT for specific time periods allowed us to define the period of Notch inactivation that is required for a permanent commitment to differentiate. Inactivation of Notch signaling revealed a cascade of proneural bHLH transcription factor gene expression that correlates with stages in progenitor cell differentiation. Microarray/QPCR analysis confirms the changes in Notch signaling components, and reveals new molecular targets for investigating neuronal differentiation. Thus, transient inactivation of Notch signaling synchronizes progenitor cell differentiation, and allows for a systematic analysis of key steps in this process. Author Affiliation: (a) Department of Biological Structure, Box 357420, University of Washington, Seattle, WA 98195, USA (b) Neurobiology and Behavior Program, University of Washington, Seattle, WA 98195, USA (c) The Research Institute for Children, Children's Hospital, New Orleans, LA 70118, USA Article History: Received 11 July 2006; Revised 23 December 2006; Accepted 2 January 2007

A transmembrane protein tyrosine phosphatase, IA-2beta, acts as an autoantigen in association with another autoantigen expressed in diabetes mellitus. IA-2beta has a structure that is only partially identical to the other diabetes autoantigen, but both were found to immunoprecipitate in reaction to diabetes sera. Exposure of both antigens to trypsin yielded fragments that may be autoantigens which signal autoimmune attack of the pancreatic islet cells.

Conrad et al conducted a study regarding the viral etiology of type 1 diabetes mellitus and the suggestion that the pancreatic beta cell damage was influenced by autoreactive T lymphocytes activated by a retroviral superantigen. Their study showed the cloning of a superantigen encoded by the envelope gene of the endogenous retrovirus HERV-K10, IDDMK(sub 1,2)22. However, the absolute specificity of IDDMK(sub 1,2)22 viremia in diabetic patients was still not confirmed.

Background: Insulinoma associated-1 (INSM1) gene is expressed exclusively in early embryonic neuroendocrine tissues, but has been found highly re-activated in most of the neuroendocrine tumors including small cell lung carcinoma.Methods: In order to elucidate the functional effects of INSM1 in normal lung development, we used a conditional lung-specific INSM1 transgenic mouse model. Transgenic (Tet-on system) CMV-INSM1 responder mice were bred with the lung-specific, club cell secretory protein (CCSP) promoter-rtTA activator mice to produce bi-transgenic progeny carrying both alleles, CCSP-rtTA and Tet-on-INSM1. Mice were fed with doxycycline containing food at the initial mating day to the postnatal day 21. Lung samples were collected at embryonic day 17.5, newborn, and postnatal day 21 for analyses.Results: Northern blot, RT-PCR, and immunohistochemical analyses revealed that doxycycline induced respiratory epithelium-specific INSM1 expression in bi-transgenic mice. Samples from postnatal day 21 mice revealed a larger lung size in the bi-transgenic mouse as compared to the single-transgenic or wild-type littermates. The histopathology results showed that the alveolar space in the bi-transgenic mice were 4 times larger than those in the single transgenic or wild-type littermates. In contrast, the size was not significantly different in the lungs collected at E17.5 or newborn among the bi-transgenic, single transgenic, or wild type mice. The respiratory epithelium with INSM1 ectopic expression suppressed cyclin D1 signal. Further in vitro studies revealed that the ectopic expression of INSM1 suppresses cyclin D1 expression and delays cell cycle progression.Conclusion: The current study suggests that CCSP promoter-driven INSM1 ectopic expression impairs normal lung development especially in postnatal alveologenesis. [ABSTRACT FROM AUTHOR]