Charla, E. Mercer, J. Maffia, P. Nicklin, S.A.
Published in
Cellular Signalling
• Extracellular vesicles are secreted under physiological and pathological conditions. • They participate in cellular signalling via transfer of their cargo. • They may contribute to all stages of atherosclerotic lesion progression. • Circulating extracellular vesicles could serve as biomarkers. • Extracellular vesicles could be used as therapeutic...
McFall, Aisling Nicklin, Stuart A. Work, Lorraine M.
Published in
Cellular Signalling
• There is an unmet need for novel therapies for treating ischaemic stroke. • The brain renin angiotensin system (RAS) provides a target for stroke treatment. • Cellular signalling via the counter regulatory RAS axis may aid brain repair. • Stimulating counter regulatory RAS is beneficial in preclinical stroke models. • Timing and route of delivery...
Poduri, Ramarao Joshi, Gaurav Jagadeesh, Gowraganahalli
Published in
Cellular signalling
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a positive-sense, single-stranded RNA virus that causes the potentially lethal Covid-19 respiratory tract infection. It does so by binding to host cell angiotensin converting enzyme 2 (ACE2) receptors, leading to endocytosis with the receptor, and subsequently using the host cell's...
Dhyani, Vaibhav Gare, Suman Gupta, Rishikesh Kumar Swain, Sarpras Venkatesh, K V Giri, Lopamudra
Published in
Cellular signalling
G-protein coupled receptor (GPCR) mediated calcium (Ca2+)-signaling transduction remains crucial in designing drugs for various complex diseases including neurodegeneration, chronic heart failure as well as respiratory diseases. Although there are several reviews detailing various aspects of Ca2+-signaling such as the role of IP3 receptors and Ca2+...
Imre, Gergely
Published in
Cellular Signalling
• Viruses selectively trigger pathogen recognition receptors, which can lead to cell death in a context dependent manner. • Apoptosis is a non immune-stimulatory cell death, which represents an anti-viral mechanism in many cases. • Necroptosis, a lytic cell death modality, is activated in response to detection of viral nucleotids and limits viral s...
Heissig, Beate Salama, Yousef Takahashi, Satoshi Osada, Taro Hattori, Koichi
Published in
Cellular Signalling
• The fibrinolytic factor plasmin interconnects with the coagulation and complement system. • Plasmin modulates macrophage functions: migration, phagocytosis. • Tissue-type plasminogen activator via LRP1 modulates TLR function. • Plasminogen/plasmin regulate efferocytosis and macrophage M1/M2 polarization during inflammation resolution. • Plasmin i...
Tachie-Menson, Theresa Gázquez-Gutiérrez, Ana Fulcher, Luke J. Macartney, Thomas J. Wood, Nicola T. Varghese, Joby Gourlay, Robert Soares, Renata F. Sapkota, Gopal P.
Published in
Cellular Signalling
• FAM83H interacts with CK1 isoforms through its DUF1669 domain and NCK1/2 through its C-terminus. • FAM83H AI mutants retain interaction with CK1 but lose interaction with NCK1/2. • Unlike wild type FAM83H, the AI mutants and associated CK1 isoforms localise mainly to the nucleus. • CK1 associated with FAM83H AI mutants retains catalytic activity....
Chen, Xuesong Geiger, Jonathan D.
Published in
Cellular Signalling
• Chloroquine (CQ) and hydroxychloroquine (HCQ) de-acidify acidic organelles and alter cell biology. • De-acidifying effects of CQ and HCQ disturb SARS-CoV2 viral biology. • De-acidifying effects of CQ and HCQ affect immune responses.
Thompson, Karen J Tobin, Andrew B
Published in
Cellular signalling
Alzheimer's disease (AD) is a neurodegenerative disorder which accounts for 60-70% of the 50 million worldwide cases of dementia and is characterised by cognitive impairments, many of which have long been associated with dysfunction of the cholinergic system. Although the M1 muscarinic acetylcholine receptor (mAChR) is considered a promising drug t...
Krześniak, Małgorzata Zajkowicz, Artur Gdowicz-Kłosok, Agnieszka Głowala-Kosińska, Magdalena Łasut-Szyszka, Barbara Rusin, Marek
Published in
Cellular Signalling
• Actinomycin D and nutlin-3a strongly and synergistically activate p53 protein • Strongly activated p53 promotes expression of innate immunity genes • Strong activation of innate immunity genes can be prevented by C16 compound • By inducing SOCS1 protein p53 can prevent overactivation of interferon signaling • Strongly activated p53 can send signa...