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The author outline a approach and policy to facilitate change in culture of cell line authentication. Topics discussed include the importance of quality control of cell lines used in biomedical research to ensure reproducibility, use of genetic signature to achieve cell line authentication and formation of the International Cell Line Authentication Committee for short tandem repeat profiling.

Upon engagement of the B Cell Receptor (BCR) of WEHI 231 immature B cells, a drop in c-Myc expression is followed by activation of the cyclin-dependent kinase inhibitor (CKI) p27Kip1, which induces growth arrest and apoptosis. Here, we report inverse patterns of p27 and c-Myc protein expression follow BCR engagement. We present evidence demonstrating, for the first time, that the p27Kip1 gene is a target of transcriptional repression by c-Myc. Specifically, the changes in p27 protein levels correlated with changes in p27 mRNA levels, and gene transcription. Induction of p27 promoter activity followed BCR engagement of WEHI 231 cells, and this induction could be repressed upon co-transfection of a c-Myc expression vector. Inhibition of the TATA-less p27 promoter by c-Myc was also observed in Jurkat T cells, vascular smooth muscle, and Hs578T breast cancer cells, extending the observation beyond immune cells. Consistent with a putative Inr element CCAGACC (where +1 is underlined) at the start site of transcription in the p27 promoter, deletion of Myc homology box II reduced the extent of repression. Furthermore, enhanced repression was observed upon transfection of the c-Myc ‘super-repressor’, with mutation of Phe115 to Leu. The sequences mediating transcriptional activity and c-Myc repression were mapped to bp -20 to +20 of the p27 gene. Finally, binding of Max was shown to facilitate c-Myc binding and repression of p27 promoter activity. Overall, these studies identify the p27 CKI gene as a new target whereby c-Myc can control cell proliferation, survival and neoplastic transformation. Oncogene (2001) 20, 1688–1702. [ABSTRACT FROM AUTHOR]

PML and Tif1a are fused to RARA and Braf, respectively, resulting in the production of PML-RARα and Tif1α-B-Raf (T18) oncoproteins. Here we show that PML, Tif1α and RXRα/RARα function together in a transcription complex that is dependent on retinoic acid (RA). We found that PML acts as a ligand-dependent coactivator of RXRα/RARα. PML interacts with Tif1α and CBP. In Pml?/? cells, the RA-dependent induction of genes such as RARB2 and the ability of Tif1α and CBP to act as transcriptional coactivators on RA are impaired. We show that both PML and Tif1α are growth suppressors required for the growth-inhibitory activity of RA. T18, similar to PML-RARα, disrupts the RA-dependent activity of this complex in a dominant-negative manner resulting in a growth advantage. Our data define a new pathway for the control of cell growth and tumorigenesis, and provide a new model for the pathogenesis of acute promyelocytic leukaemia (APL). [ABSTRACT FROM AUTHOR]

Presents research which reported 13 ligand-dependent proteins called DRIPs and their function in hormone-dependent transactivation by vitamin D receptor (VDR) on chromatin templates. Role of nuclear receptors in gene transcription; Effects of binding to ligands; DRIP binding; DRIPs compared with the cofactor complex ARC; Other DRIP/ARC subunits; Role of nuclear-receptor ligands.

A letter to the editor is presented in response to an article by A. Bradbury and colleagues published in the journal in 2015, which focuses on recombinant antibodies.