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Welcome to BJ Signal

Discover what's new and interesting in all aspects of signalling

This latest Themed Collection from Portland Press highlights a selection of recent high-quality papers concerning various aspects of signalling that have been published in our family of journals (Biochemical Journal, Biochemical Society Transactions, Bioscience Reports and Clinical Science).
One of the key areas of biochemistry is signalling, both within the cell, across the cell membrane and between cells. The selected papers here cover a wide range of topics including receptors, redox signalling, signalling pathways involved in cancer, responses and regulation of signalling pathways, and the clinical impact of neurological signalling pathway interference.
This diverse collection of papers emphasizes the importance of signalling systems in a wide array of scientific disciplines, and we welcome the submission of research articles on all aspects of signalling to the Portland Press family of journals. These papers are freely available for 3 months.
Vascular smooth muscle plays a key role in pathophysiology of cardiovascular diseases and recently, vascular smooth muscle cells (VSMCs) have been used therapeutically for vascular regeneration, although limitations include the source and number of cells available to clinicians. Induced pluripotent stem cell (iPSC) technology can be used to reprogram adult cells to an earlier pluripotent state.
In this review, Dash et al first discuss the recent iPSC technology and vascular smooth muscle development from an embryo and then examine different methodologies to derive VSMCs from iPSCs. IPSC-derived VMSCs can then be used in applications such as disease modelling, VSMCs offering a unique and alternative way of studying the earlier stages of the disease in a human context, as well as highlighting therapeutic opportunities for the construction of tissue-engineered blood vessels.
The cAMP signalling pathway plays an essential role in immune functions. This recent study from Xiaodong Cheng and colleagues examines the role of the cAMP/EPAC1 (exchange protein directly activated by cAMP) axis in regulatory T-cell (Treg)-mediated immunosuppression using genetic and pharmacological approaches.
Cheng et al. found that EPAC1 inhibition enhanced activation of the transcription factor STAT3 and up-regulated SMAD7 expression while down-regulating expression of SMAD4, desensitising CD4+ T cells to transforming growth factor (TGF) β1. These in vivo observations are consistent with the finding that EPAC1 plays an important role in Treg-mediated suppression. Cheng et al showed that EPAC1 boosts Treg-mediated suppression, and identified EPAC1 as a therapeutic target, with Tregs are involved in numerous pathologies, including autoimmunity, infections and a wide range of cancers.
Glycogen synthase kinase 3 (GSK3) is essential for normal development and function of the central nervous system. It is especially important for regulating neurotransmission, although the downstream substrates mediating this function are not yet clear. In this paper, Graham Neely, Adam Cole and colleagues report that the lipid kinase phosphatidylinositol 4-kinase II α (PI4KIIα) is a novel substrate of GSK3 that regulates trafficking and cell-surface expression of neurotransmitter receptors in neurons. Their studies implicate signalling between GSK3 and PI4KIIα as a novel regulator of vesicular trafficking and neurotransmission in the brain.
Content in BJ Signal
2015 - Volumes 465-472
  • Volume 465
    • part 3, 359-515 (1 Feb)
    • part 2, 185-357 (15 Jan)
    • part 1, 1-184 (1 Jan)
2014 - Volumes 457-464
  • Volume 464
    • part 3, 293-472 (15 Dec)
    • part 2, 169-291 (1 Dec)
    • part 1, 1-168 (15 Nov)
  • Volume 463
    • part 3, 319-437 (1 Nov)
    • part 2, 167-317 (15 Oct)
    • part 1, 1-165 (1 Oct)
2013 - Volumes 449-456
2012 - Volumes 441-448
  • Volume 448
    • part 3, 297-423 (15 Dec)
    • part 2, 171-295 (1 Dec)
    • part 1, 1-169 (15 Nov)
2011 - Volumes 433-440
2010 - Volumes 425-432
  • Volume 430
    • part 3, 365-599 (15 Sep)
    • part 2, 179-364 (1 Sep)
    • part 1, 1-177 (15 Aug)
2009 - Volumes 417-424
2008 - Volumes 409-416
2007 - Volumes 401-408
2006 - Volumes 393-400
2005 - Volumes 385-392
2004 - Volumes 377-384
2003 - Volumes 369-376
  • Volume 369
    • part 3, 429-739 (1 Feb)
    • part 2, 199-427 (15 Jan)
    • part 1, 1-198 (1 Jan)
2002 - Volumes 361-368