A simple proposal for the publication of journal citation distributions

Although the Journal Impact Factor (JIF) is widely acknowledged to be a poor indicator of the quality of individual papers, it is used routinely to evaluate research and researchers. Here, we present a simple method for generating the citation distributions that underlie JIFs. Application of this straightforward protocol reveals the full extent of the skew of these distributions and the variation in citations received by published papers that is characteristic of all scientific journals. Although there are differences among journals across the spectrum of JIFs, the citation distributions overlap extensively, demonstrating that the citation performance of individual papers cannot be inferred from the JIF. We propose that this methodology be adopted by all journals as a move to greater transparency, one that should help to refocus attention on individual pieces of work and counter the inappropriate usage of JIFs during the process of research assessment

Caractérisation d'une région régulatrice de l'expression du virus de la leucémie bovine située en aval du site d'initiation de la transcription

Doctorat en Sciencesinfo:eu-repo/semantics/nonPublishe

Caractérisation d'une région régulatrice de l'expression du virus de la leucémie bovine située en aval du site d'initiation de la transcription

Doctorat en Sciencesinfo:eu-repo/semantics/nonPublishe

The emerging role of class II histone deacetylases.

Histone acetylation and deacetylation play essential roles in modifying chromatin structure and regulating gene expression in all eukaryotes. Several histone acetyltransferases have been identified that act as transcriptional coactivators. In contrast, histone deacetylases (HDACs) are part of transcriptional corepressor complexes. Based on their similarity to known yeast factors, the human HDACs are grouped into three classes. Class I HDACs are similar to the yeast transcriptional repressor yRPD3, while class II HDACs are related to yHDA1 and class III HDACs to ySIR2. In this review, we focus on the biology of class II HDACs. These newly discovered enzymes have been implicated in cell differentiation and development, and many molecular details are emerging that shed light on class II HDAC function and regulation. We discuss the biological role of these factors in the context of physiological processes

The role of the RU5 region of the Bovine leukemia virus genome in the transcriptional control of viral expression

info:eu-repo/semantics/publishe

Regulation of gene expression by the R-U5 region of Bovine leukemia virus genome

info:eu-repo/semantics/publishe

The role of a potential c-Myc/Max binding site on the bovine leukemia virus long terminal repeat transcriptional activity

info:eu-repo/semantics/publishe

Identification and characterization of a functional E-box motif in the R region of the Bovine Leukemia Virus Long Terminal repeat

info:eu-repo/semantics/publishe

An interferon regulatory factor binding site in the U5 region of the bovine leukemia virus long terminal repeat stimulates Tax-independent gene expression

Bovine leukemia virus (BLV) replication is controlled by both cis- and trans-acting elements. The virus-encoded transactivator, Tax, is necessary for efficient transcription from the BLV promoter, although it is not present during the early stages of infection. Therefore, sequences that control Tax-independent transcription must play an important role in the initiation of viral gene expression. This study demonstrates that the R-U5 sequence of BLV stimulates Tax-independent reporter gene expression directed by the BLV promoter. R-U5 was also stimulatory when inserted immediately downstream from the transcription initiation site of a heterologous promoter. Progressive deletion analysis of this region revealed that a 46-bp element corresponding to the 5' half of U5 is principally responsible for the stimulation. This element exhibited enhancer activity when inserted upstream or downstream from the herpes simplex virus thymidine kinase promoter. This enhancer contains a binding site for the interferon regulatory factors IRF-1 and IRF-2. A 3-bp mutation that destroys the IRF recognition site caused a twofold decrease in Tax-independent BLV long terminal repeat-driven gene expression. These observations suggest that the IRF binding site in the U5 region of BLV plays a role in the initiation of virus replication.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe