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Artykuły w czasopismach na temat „Signalosomes”

Autor: Grafiati

Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Kim, Ingyu, Weijun Pan, Sara A. Jones, Youxin Zhang, Xiaowei Zhuang, and Dianqing Wu. "Clathrin and AP2 are required for PtdIns(4,5)P2-mediated formation of LRP6 signalosomes." Journal of Cell Biology 200, no. 4 (2013): 419–28. http://dx.doi.org/10.1083/jcb.201206096.

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Canonical Wnt signaling is initiated by the binding of Wnt proteins to their receptors, low-density lipoprotein-related protein 5 and 6 (LRP5/6) and frizzled proteins, leading to phosphatidylinositol (4,5)bisphosphate (PtdIns(4,5)P2) production, signalosome formation, and LRP phosphorylation. However, the mechanism by which PtdIns(4,5)P2 regulates the signalosome formation remains unclear. Here we show that clathrin and adaptor protein 2 (AP2) were part of the LRP6 signalosomes. The presence of clathrin and AP2 in the LRP6 signalosomes depended on PtdIns(4,5)P2, and both clathrin and AP2 were

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Quinlan, Casey L., Alexandre D. T. Costa, Cinthia L. Costa, Sandrine V. Pierre, Pierre Dos Santos, and Keith D. Garlid. "Conditioning the heart induces formation of signalosomes that interact with mitochondria to open mitoKATPchannels." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (2008): H953—H961. http://dx.doi.org/10.1152/ajpheart.00520.2008.

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Perfusion of the heart with bradykinin triggers cellular signaling events that ultimately cause opening of mitochondrial ATP-sensitive K+(mitoKATP) channels, increased H2O2production, inhibition of the mitochondrial permeability transition (MPT), and cardioprotection. We hypothesized that the interaction of bradykinin with its receptor induces the assembly of a caveolar signaling platform (signalosome) that contains the enzymes of the signaling pathway and that migrates to mitochondria to induce mitoKATPchannel opening. We developed a novel method for isolating and purifying signalosomes from

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3

Gerlach, Jan P., Ingrid Jordens, Daniele V. F. Tauriello, et al. "TMEM59 potentiates Wnt signaling by promoting signalosome formation." Proceedings of the National Academy of Sciences 115, no. 17 (2018): E3996—E4005. http://dx.doi.org/10.1073/pnas.1721321115.

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Wnt/β-catenin signaling controls development and adult tissue homeostasis by regulating cell proliferation and cell fate decisions. Wnt binding to its receptors Frizzled (FZD) and low-density lipoprotein-related 6 (LRP6) at the cell surface initiates a signaling cascade that leads to the transcription of Wnt target genes. Upon Wnt binding, the receptors assemble into large complexes called signalosomes that provide a platform for interactions with downstream effector proteins. The molecular basis of signalosome formation and regulation remains elusive, largely due to the lack of tools to analy

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4

Piperno, Anna, Angela Scala, Antonino Mazzaglia, et al. "Cellular Signaling Pathways Activated by Functional Graphene Nanomaterials." International Journal of Molecular Sciences 19, no. 11 (2018): 3365. http://dx.doi.org/10.3390/ijms19113365.

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The paper reviews the network of cellular signaling pathways activated by Functional Graphene Nanomaterials (FGN) designed as a platform for multi-targeted therapy or scaffold in tissue engineering. Cells communicate with each other through a molecular device called signalosome. It is a transient co-cluster of signal transducers and transmembrane receptors activated following the binding of transmembrane receptors to extracellular signals. Signalosomes are thus efficient and sensitive signal-responding devices that amplify incoming signals and convert them into robust responses that can be rel

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5

Tulsian, Nikhil K., Valerie Jia-En Sin, Hwee-Ling Koh, and Ganesh S. Anand. "Development of Phosphodiesterase–Protein-Kinase Complexes as Novel Targets for Discovery of Inhibitors with Enhanced Specificity." International Journal of Molecular Sciences 22, no. 10 (2021): 5242. http://dx.doi.org/10.3390/ijms22105242.

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Phosphodiesterases (PDEs) hydrolyze cyclic nucleotides to modulate multiple signaling events in cells. PDEs are recognized to actively associate with cyclic nucleotide receptors (protein kinases, PKs) in larger macromolecular assemblies referred to as signalosomes. Complexation of PDEs with PKs generates an expanded active site that enhances PDE activity. This facilitates signalosome-associated PDEs to preferentially catalyze active hydrolysis of cyclic nucleotides bound to PKs and aid in signal termination. PDEs are important drug targets, and current strategies for inhibitor discovery are ba

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6

Song, Wenxia, Chaohong Liu, Heather Miller, et al. "BCR-induced actin rearrangement provides a driving force for the formation of surface BCR signalosomes (84.1)." Journal of Immunology 184, no. 1_Supplement (2010): 84.1. http://dx.doi.org/10.4049/jimmunol.184.supp.84.1.

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Abstract In response to antigens, the BCR forms surface signalosomes where it initiates signaling cascades and antigen internalization. This study examines the role of the actin cytoskeleton in BCR signalosome formation. Both multi-valent soluble and membrane-associated antigens induce BCR clustering and actin reorganization. Actin is actively polymerized at BCR microclusters upon their formation and surrounding BCR clusters as they are merged into central clusters. Actin regulators, WASP, cofilin and gelsolin, are activated and recruited to BCR clusters. Latrunculin or jasplakinolide treatmen

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7

Negro, Alejandra, Kimberly Dodge-Kafka, and Michael S. Kapiloff. "Signalosomes as therapeutic targets." Progress in Pediatric Cardiology 25, no. 1 (2008): 51–56. http://dx.doi.org/10.1016/j.ppedcard.2007.11.012.

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8

Nhieu, Jennifer, Fatimah Najjar, and Li-Na Wei. "CRABP1 Signalosomes in Non-Canonical Actions of Retinoic Acid—Maintaining Health and Preventing Thyroid Dysfunction in Aging." Endocrines 6, no. 2 (2025): 26. https://doi.org/10.3390/endocrines6020026.

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Retinoic acid (RA) exerts biological effects through RA receptors (RARs) to regulate transcription. RA also elicits rapid, RAR-independent (noncanonical) activities mediated by Cellular RA Binding Protein 1 (CRABP1) to modulate cytosolic signaling. CRABP1 functions by forming protein complexes, named CRABP1 signalosomes, to modulate signal propagation in a cell type-specific manner. This review summarizes multiple CRABP1 signalosomes and their physiological functions. CRABP1 knockout (CKO) mice develop multiple phenotypes progressively throughout the lifespan. These include altered brain funct

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9

Tulsian, Nikhil K., Abhijeet Ghode, and Ganesh S. Anand. "Adenylate control in cAMP signaling: implications for adaptation in signalosomes." Biochemical Journal 477, no. 16 (2020): 2981–98. http://dx.doi.org/10.1042/bcj20200435.

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In cAMP-Protein Kinase A (PKA) signaling, A-kinase anchoring protein scaffolds assemble PKA in close proximity to phosphodiesterases (PDE), kinase-substrates to form signaling islands or ‘signalosomes’. In its basal state, inactive PKA holoenzyme (R2:C2) is activated by binding of cAMP to regulatory (R)-subunits leading to dissociation of active catalytic (C)-subunits. PDEs hydrolyze cAMP-bound to the R-subunits to generate 5′-AMP for termination and resetting the cAMP signaling. Mechanistic basis for cAMP signaling has been derived primarily by focusing on the proteins in isolation. Here, we

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10

Abdel-Nour, Mena, Leticia A. M. Carneiro, Jeffrey Downey, et al. "The heme-regulated inhibitor is a cytosolic sensor of protein misfolding that controls innate immune signaling." Science 365, no. 6448 (2019): eaaw4144. http://dx.doi.org/10.1126/science.aaw4144.

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Multiple cytosolic innate sensors form large signalosomes after activation, but this assembly needs to be tightly regulated to avoid accumulation of misfolded aggregates. We found that the eIF2α kinase heme-regulated inhibitor (HRI) controls NOD1 signalosome folding and activation through a process requiring eukaryotic initiation factor 2α (eIF2α), the transcription factor ATF4, and the heat shock protein HSPB8. The HRI/eIF2α signaling axis was also essential for signaling downstream of the innate immune mediators NOD2, MAVS, and TRIF but dispensable for pathways dependent on MyD88 or STING. M

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11

Minton, Kirsty. "Stress response to innate immune signalosomes." Nature Reviews Immunology 19, no. 9 (2019): 534–35. http://dx.doi.org/10.1038/s41577-019-0201-0.

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Minton, Kirsty. "NF-κB signalosomes on the ER". Nature Reviews Immunology 13, № 10 (2013): 706. http://dx.doi.org/10.1038/nri3543.

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13

Mund, Thomas, Michael Graeb, Juliusz Mieszczanek, Melissa Gammons, Hugh R. B. Pelham, and Mariann Bienz. "Disinhibition of the HECT E3 ubiquitin ligase WWP2 by polymerized Dishevelled." Open Biology 5, no. 12 (2015): 150185. http://dx.doi.org/10.1098/rsob.150185.

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Dishevelled is a pivot in Wnt signal transduction, controlling both β-catenin-dependent transcription to specify proliferative cell fates, and cell polarity and other non-nuclear events in post-mitotic cells. In response to Wnt signals, or when present at high levels, Dishevelled forms signalosomes by dynamic polymerization. Its levels are controlled by ubiquitylation, mediated by various ubiquitin ligases, including NEDD4 family members that bind to a conserved PPxY motif in Dishevelled (mammalian Dvl1–3). Here, we show that Dvl2 binds to the ubiquitin ligase WWP2 and unlocks its ligase activ

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14

Rawlings, David J. "The biology and biochemistry of inflammatory signalosomes." EMBO reports 7, no. 1 (2006): 25–30. http://dx.doi.org/10.1038/sj.embor.7400599.

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15

Torres-Quesada, Omar, Johanna E. Mayrhofer, and Eduard Stefan. "The many faces of compartmentalized PKA signalosomes." Cellular Signalling 37 (September 2017): 1–11. http://dx.doi.org/10.1016/j.cellsig.2017.05.012.

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16

Zhang, Chun, and Pin-Lan Li. "Membrane raft redox signalosomes in endothelial cells." Free Radical Research 44, no. 8 (2010): 831–42. http://dx.doi.org/10.3109/10715762.2010.485994.

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17

Record, Michel, Caroline Subra, Sandrine Silvente-Poirot, and Marc Poirot. "Exosomes as intercellular signalosomes and pharmacological effectors." Biochemical Pharmacology 81, no. 10 (2011): 1171–82. http://dx.doi.org/10.1016/j.bcp.2011.02.011.

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18

Lichtenstein, Mauriz A., Fakun Cao, Finn Lobnow, et al. "Bottom-up reconstruction of functional death fold signalosomes reveals a requirement for polymer stability and avidity." Science 388, no. 6745 (2025): 415–22. https://doi.org/10.1126/science.adq3234.

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Protein polymer scaffolds composed of death fold (DF) proteins are critical to the formation of signalosomes in immune signaling. The biophysical properties that these polymeric scaffolds require for signal transduction are not clearly defined. Here, we engineered single-component DF signalosomes. We found that functionality depends on the stability provided by the DF polymer, which could also be achieved with a bacterial DF domain, a synthetic filament-forming domain, and amyloid-like sequences. This demonstrates the importance of polymer stability and inducibility irrespective of the motif’s

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19

Monterisi, Stefania, and Manuela Zaccolo. "Components of the mitochondrial cAMP signalosome." Biochemical Society Transactions 45, no. 1 (2017): 269–74. http://dx.doi.org/10.1042/bst20160394.

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3′-5′-Cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) signalling is activated by different extracellular stimuli and mediates many diverse processes within the same cell. It is now well established that in order to translate into the appropriate cellular function multiple extracellular inputs, which may act simultaneously on the same cell, the cAMP/PKA signalling pathway is compartmentalised. Multimolecular complexes are organised at specific subcellular sites to generate spatially confined signalosomes, which include effectors, modulators and targets of the pathway. In recent years

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20

Murphy, Elizabeth, Renee Wong, and Charles Steenbergen. "Signalosomes: delivering cardioprotective signals from GPCRs to mitochondria." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (2008): H920—H922. http://dx.doi.org/10.1152/ajpheart.00738.2008.

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Traver, Maria K., Leonard Campanello, Suman Paul, Hari Shroff, Wolfgang Losert та Brian C. Schaefer. "Coalescence of Nanoscale Cytoplasmic Signalosomes Contributes to T Cell Receptor Signaling to NF-κB". Journal of Immunology 198, № 1_Supplement (2017): 52.13. http://dx.doi.org/10.4049/jimmunol.198.supp.52.13.

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Abstract T cell receptor (TCR) activation of the transcription factor NF-κB is a crucial determinant of effector T lymphocyte function. The complex regulatory network surrounding this pathway remains poorly understood, particularly at time periods further removed from initial TCR triggering. We have previously demonstrated that following activation of the TCR, the proteins p62, Bcl10, and Malt1 rapidly combine to form a cytoplasmic filamentous signalosome called POLKADOTS, which recruits further signaling proteins and initiates the terminal steps in activation of NF-κB. Here, we examine the fa

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22

Cattaruzza, Fiore, Daniel P. Poole, and Nigel W. Bunnett. "Arresting inflammation: contributions of plasma membrane and endosomal signalling to neuropeptide-driven inflammatory disease." Biochemical Society Transactions 41, no. 1 (2013): 137–43. http://dx.doi.org/10.1042/bst20120343.

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GPCR (G-protein-coupled receptor) signalling at the plasma membrane is under tight control. In the case of neuropeptides such as SP (substance P), plasma membrane signalling is regulated by cell-surface endopeptidases (e.g. neprilysin) that degrade extracellular neuropeptides, and receptor interaction with β-arrestins, which uncouple receptors from heterotrimeric G-proteins and mediate receptor endocytosis. By recruiting GPCRs, kinases and phosphatases to endocytosed GPCRs, β-arrestins assemble signalosomes that can mediate a second wave of signalling by internalized receptors. Endosomal pepti

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23

Awasthi, Aradhana, Asanga Samarakoon, Haiyan Chu, et al. "Rap1b facilitates NK cell functions via IQGAP1-mediated signalosomes." Journal of Experimental Medicine 207, no. 9 (2010): 1923–38. http://dx.doi.org/10.1084/jem.20100040.

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Rap1 GTPases control immune synapse formation and signaling in lymphocytes. However, the precise molecular mechanism by which Rap1 regulates natural killer (NK) cell activation is not known. Using Rap1a or Rap1b knockout mice, we identify Rap1b as the major isoform in NK cells. Its absence significantly impaired LFA1 polarization, spreading, and microtubule organizing center (MTOC) formation in NK cells. Neither Rap1 isoform was essential for NK cytotoxicity. However, absence of Rap1b impaired NKG2D, Ly49D, and NCR1-mediated cytokine and chemokine production. Upon activation, Rap1b colocalized

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Wegener, E., and D. Krappmann. "CARD-Bcl10-Malt1 Signalosomes: Missing Link to NF- B." Science's STKE 2007, no. 384 (2007): pe21. http://dx.doi.org/10.1126/stke.3842007pe21.

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Molano, Alberto, and Simin Nikbin Meydani. "Vitamin E, signalosomes and gene expression in T cells." Molecular Aspects of Medicine 33, no. 1 (2012): 55–62. http://dx.doi.org/10.1016/j.mam.2011.11.002.

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Huber, Thomas, Alexandre Fürstenberg, He Tian, Hubert F. Gaertner, Oliver Hartley, and Thomas P. Sakmar. "Multi-Color, Single-Molecule Fluorescence Imaging of GPCR Signalosomes." Biophysical Journal 106, no. 2 (2014): 238a. http://dx.doi.org/10.1016/j.bpj.2013.11.1395.

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Garlid, Keith D., and Caitlin Pesout. "Signalosomes transmit signals from plasma membrane receptors to mitochondria." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1797 (July 2010): 120. http://dx.doi.org/10.1016/j.bbabio.2010.04.359.

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Meydani, Simin Nikbin, and Melissa G. Marko. "Vitamin E, signalosomes and gene expression in T cells." Clinical Biochemistry 44, no. 13 (2011): S20. http://dx.doi.org/10.1016/j.clinbiochem.2011.08.058.

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Mendoza-Topaz, Carolina, Juliusz Mieszczanek, and Mariann Bienz. "The Adenomatous polyposis coli tumour suppressor is essential for Axin complex assembly and function and opposes Axin's interaction with Dishevelled." Open Biology 1, no. 3 (2011): 110013. http://dx.doi.org/10.1098/rsob.110013.

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Most cases of colorectal cancer are linked to mutational inactivation of the Adenomatous polyposis coli (APC) tumour suppressor. APC downregulates Wnt signalling by enabling Axin to promote the degradation of the Wnt signalling effector β-catenin (Armadillo in flies). This depends on Axin's DIX domain whose polymerization allows it to form dynamic protein assemblies (‘degradasomes’). Axin is inactivated upon Wnt signalling, by heteropolymerization with the DIX domain of Dishevelled, which recruits it into membrane-associated ‘signalosomes’. How APC promotes Axin's function is unclear, especial

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Mingueneau, Michael, Wenyu Jiang, Markus Feuerer, Diane Mathis, and Christophe Benoist. "Thymic negative selection is functional in NOD mice." Journal of Experimental Medicine 209, no. 3 (2012): 623–37. http://dx.doi.org/10.1084/jem.20112593.

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Based on analyses of multiple TCR transgenic (tg) models, the emergence of pathogenic T cells in diabetes-prone NOD mice has been ascribed to a failure to censure autoreactive clones in the thymus. In contrast, using isolated and preselected thymocytes, we show that nonobese diabetic (NOD) genetic variation impairs neither clonal deletion nor downstream transcriptional programs. However, we find that NOD genetic variation influences αβ/γδ-lineage decisions promoted by early expression of tg αβ-TCRs at the double-negative (DN) stage. In B6 and other genetic backgrounds, tg αβ-TCRs behave like γ

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Xu, Ming, Min Xia, Xiao-Xue Li, et al. "Requirement of translocated lysosomal V1 H+-ATPase for activation of membrane acid sphingomyelinase and raft clustering in coronary endothelial cells." Molecular Biology of the Cell 23, no. 8 (2012): 1546–57. http://dx.doi.org/10.1091/mbc.e11-09-0821.

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Acid sphingomyelinase (ASM) mediates the formation of membrane raft (MR) redox signalosomes in a process that depends on a local acid microenvironment in coronary arterial endothelial cells (CAECs). However, it is not known how this local acid microenvironment is formed and maintained. The present study hypothesized that lysosomal V1 H+-ATPase provides a hospitable acid microenvironment for activation of ASM when lysosomes traffic and fuse into the cell membrane. Confocal microscopy showed that local pH change significantly affected MRs, with more fluorescent patches under low pH. Correspondin

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Formoso, Karina, Frank Lezoualc’h, and Jeanne Mialet-Perez. "Role of EPAC1 Signalosomes in Cell Fate: Friends or Foes?" Cells 9, no. 9 (2020): 1954. http://dx.doi.org/10.3390/cells9091954.

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The compartmentation of signaling processes is accomplished by the assembly of protein complexes called signalosomes. These signaling platforms colocalize enzymes, substrates, and anchoring proteins into specific subcellular compartments. Exchange protein directly activated by cAMP 1 (EPAC1) is an effector of the second messenger, 3′,5′-cyclic adenosine monophosphate (cAMP) that is associated with multiple roles in several pathologies including cardiac diseases. Both EPAC1 intracellular localization and molecular partners are key players in the regulation of cell fate, which may have important

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Blair, Connor M., and George S. Baillie. "Reshaping cAMP nanodomains through targeted disruption of compartmentalised phosphodiesterase signalosomes." Biochemical Society Transactions 47, no. 5 (2019): 1405–14. http://dx.doi.org/10.1042/bst20190252.

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Abstract Spatio-temporal regulation of localised cAMP nanodomains is highly dependent upon the compartmentalised activity of phosphodiesterase (PDE) cyclic nucleotide degrading enzymes. Strategically positioned PDE–protein complexes are pivotal to the homeostatic control of cAMP-effector protein activity that in turn orchestrate a wide range of cellular signalling cascades in a variety of cells and tissue types. Unsurprisingly, dysregulated PDE activity is central to the pathophysiology of many diseases warranting the need for effective therapies that target PDEs selectively. This short review

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Bilic, J., Y. L. Huang, G. Davidson, et al. "Wnt Induces LRP6 Signalosomes and Promotes Dishevelled-Dependent LRP6 Phosphorylation." Science 316, no. 5831 (2007): 1619–22. http://dx.doi.org/10.1126/science.1137065.

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Dodge-Kafka, Kimberly L., Moriah Gildart, Jinliang Li, Hrishikesh Thakur та Michael S. Kapiloff. "Bidirectional regulation of HDAC5 by mAKAPβ signalosomes in cardiac myocytes". Journal of Molecular and Cellular Cardiology 118 (травень 2018): 13–25. http://dx.doi.org/10.1016/j.yjmcc.2018.03.001.

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Hara, Yu, Fumiaki Ando, Hideki Yanagawa, et al. "LRBA Signalosomes Activate Vasopressin-Induced AQP2 Trafficking at Recycling Endosomes." Journal of the American Society of Nephrology 34, no. 11S (2023): 543. http://dx.doi.org/10.1681/asn.20233411s1543c.

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Song, Wenxia, Margaret Seeley-Fallen, Olusegun Onabajo, Tse-Hua Tan, and Arpita Upadhyaya. "Actin-binding protein 1 links B-cell receptor to negative signaling pathways (IRC3P.462)." Journal of Immunology 192, no. 1_Supplement (2014): 59.5. http://dx.doi.org/10.4049/jimmunol.192.supp.59.5.

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Abstract Prolonged or uncontrolled B-cell receptor (BCR) signaling is associated with autoimmunity. We previously demonstrated a role for actin in BCR signal attenuation. This study reveals that Actin-binding protein 1 (Abp1/HIP-55/SH3P7) is a critical negative regulator of BCR signaling, and is responsible for linking actin remodeling to negative regulatory pathways of the BCR. In Abp1 knockout mice, the numbers of spontaneous germinal center B cells and marginal zone B cells are significantly increased, while early B-cell development is unaltered. Serum levels of autoantibody and total antib

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Mayans, Olga, Guy M. Benian, Felix Simkovic, and Daniel J. Rigden. "Mechanistic and functional diversity in the mechanosensory kinases of the titin-like family." Biochemical Society Transactions 41, no. 4 (2013): 1066–71. http://dx.doi.org/10.1042/bst20130085.

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The giant cytoskeletal kinases of the titin-like family are emerging as key mediators of stretch-sensing in muscle. It is thought that their elastic conformational deformation during muscle function regulates both their catalysis and the recruitment of regulatory proteins to signalosomes that assemble in their vicinity. In the present article, we discuss the speciation of mechanosensory mechanisms in titin-like kinases, their scaffolding properties and the kinase/pseudokinase domain variations that define a rich functional diversity across the family.

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Heussler, V. T., S. Rottenberg, R. Schwab, et al. "Hijacking of Host Cell IKK Signalosomes by the Transforming Parasite Theileria." Science 298, no. 5595 (2002): 1033–36. http://dx.doi.org/10.1126/science.1075462.

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Roncagalli, Romain, Michael Mingueneau, Claude Grégoire, Christelle Langlet, Bernard Malissen, and Marie Malissen. "Lymphoproliferative disorders involving T helper effector cells with defective LAT signalosomes." Seminars in Immunopathology 32, no. 2 (2010): 117–25. http://dx.doi.org/10.1007/s00281-009-0195-y.

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Satpathy, Shankha, Sebastian A. Wagner, Petra Beli, et al. "Systems‐wide analysis of BCR signalosomes and downstream phosphorylation and ubiquitylation." Molecular Systems Biology 11, no. 6 (2015): 810. http://dx.doi.org/10.15252/msb.20145880.

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Laudanna, Carlo, and Ronen Alon. "Right on the spot." Thrombosis and Haemostasis 95, no. 01 (2006): 5–11. http://dx.doi.org/10.1160/th05-07-0482.

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SummaryThe arrest of rolling leukocytes on various target vascular beds is crucial for their recruitment at inflammatory sites and secondary lymphoid tissues. Leukocyte arrest is predominantly mediated by integrins interacting with either constitutive or inducible endothelial ligands. Integrins are cytoskeletally regulated heterodimers maintained in largely low affinity conformational states on circulating leukocytes. For arrest to occur, the affinity of integrin heterodimers must be enhanced in situ upon leukocyte encounter with proper endothelial-displayed chemokines or chemoattractants whic

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Zhou, Lihong, and Felicity Z. Watts. "Nep1, a Schizosaccharomyces pombe deneddylating enzyme." Biochemical Journal 389, no. 2 (2005): 307–14. http://dx.doi.org/10.1042/bj20041991.

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Nedd8 is a ubiquitin-like modifier that is attached to the cullin components of E3 ubiquitin ligases. More recently, p53 has also been shown to be Nedd8-modified. Nedd8 attachment occurs in a manner similar to that observed for other ubiquitin-like modifiers. In the present study, we report on the characterization of Nep1, a deneddylating enzyme in fission yeast (Schizosaccharomyces pombe). Unlike loss of ned8, deletion of the nep1 gene is not lethal, although nep1.d cells are heterogeneous in length, suggesting a defect in cell-cycle progression. Viability of nep1.d cells is dependent on a fu

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Lin Jian, 林健, та 陈鑫 Chen Xin. "关键生物信号枢纽的细胞原位单分子定位超高分辨率解析". Chinese Journal of Lasers 51, № 3 (2024): 0307103. http://dx.doi.org/10.3788/cjl231390.

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Wu, Hao, and Monika Fuxreiter. "The Structure and Dynamics of Higher-Order Assemblies: Amyloids, Signalosomes, and Granules." Cell 165, no. 5 (2016): 1055–66. http://dx.doi.org/10.1016/j.cell.2016.05.004.

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Kirchhof, Mark G., Luan A. Chau, Caitlin D. Lemke, et al. "Stomatin-Like Protein 2 Sustains Signalling from T Cell Receptor Signalosomes (87.36)." Journal of Immunology 178, no. 1_Supplement (2007): S134—S135. http://dx.doi.org/10.4049/jimmunol.178.supp.87.36.

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Abstract T cell activation involves the formation of an organized interface between the T cell and the antigen-presenting cell known as the immunological synapse (IS). Sustained T cell signalling at the IS emanates from peripheral supramolecular activating complexes (pSMACs). We hypothesized that a molecular machinery would anchor the TCR microclusters in the periphery of the synapse to the cytoskeleton allowing the recruitment of signalosome components and providing sustained TCR signalling. Here, we report that stomatin-like protein-2 (SLP-2) is a key element of this machinery by linking the

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Paolillo, Roberta, Stefania D’Apice, Gabriele Giacomo Schiattarella, et al. "Mitochondrial a Kinase Anchor Proteins in Cardiovascular Health and Disease: A Review Article on Behalf of the Working Group on Cellular and Molecular Biology of the Heart of the Italian Society of Cardiology." International Journal of Molecular Sciences 23, no. 14 (2022): 7691. http://dx.doi.org/10.3390/ijms23147691.

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Second messenger cyclic adenosine monophosphate (cAMP) has been found to regulate multiple mitochondrial functions, including respiration, dynamics, reactive oxygen species production, cell survival and death through the activation of cAMP-dependent protein kinase A (PKA) and other effectors. Several members of the large family of A kinase anchor proteins (AKAPs) have been previously shown to locally amplify cAMP/PKA signaling to mitochondria, promoting the assembly of signalosomes, regulating multiple cardiac functions under both physiological and pathological conditions. In this review, we w

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Li, Jinliang, Yuliang Tan, Catherine L. Passariello, et al. "Signalosome-Regulated Serum Response Factor Phosphorylation Determining Myocyte Growth in Width Versus Length as a Therapeutic Target for Heart Failure." Circulation 142, no. 22 (2020): 2138–54. http://dx.doi.org/10.1161/circulationaha.119.044805.

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Background: Concentric and eccentric cardiac hypertrophy are associated with pressure and volume overload, respectively, in cardiovascular disease both conferring an increased risk of heart failure. These contrasting forms of hypertrophy are characterized by asymmetrical growth of the cardiac myocyte in mainly width or length, respectively. The molecular mechanisms determining myocyte preferential growth in width versus length remain poorly understood. Identification of the mechanisms governing asymmetrical myocyte growth could provide new therapeutic targets for the prevention or treatment of

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EL FAR, Oussama, and Heinrich BETZ. "G-protein-coupled receptors for neurotransmitter amino acids: C-terminal tails, crowded signalosomes." Biochemical Journal 365, no. 2 (2002): 329–36. http://dx.doi.org/10.1042/bj20020481.

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G-protein-coupled receptors (GPCRs) represent a superfamily of highly diverse integral membrane proteins that transduce external signals to different subcellular compartments, including nuclei, via trimeric G-proteins. By differential activation of diffusible Gα and membrane-bound Gβγ subunits, GPCRs might act on both cytoplasmic/intracellular and plasma-membrane-bound effector systems. The coupling efficiency and the plasma membrane localization of GPCRs are regulated by a variety of interacting proteins. In this review, we discuss recently disclosed protein interactions found with the cytopl

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Bhatt, Akansha, Biswa P. Mishra, Weixi Gu, et al. "Structural characterization of TIR-domain signalosomes through a combination of structural biology approaches." IUCrJ 11, no. 5 (2024): 695–707. http://dx.doi.org/10.1107/s2052252524007693.

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The TIR (Toll/interleukin-1 receptor) domain represents a vital structural element shared by proteins with roles in immunity signalling pathways across phyla (from humans and plants to bacteria). Decades of research have finally led to identifying the key features of the molecular basis of signalling by these domains, including the formation of open-ended (filamentous) assemblies (responsible for the signalling by cooperative assembly formation mechanism, SCAF) and enzymatic activities involving the cleavage of nucleotides. We present a historical perspective of the research that led to this u

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