Journal articles: 'Oligomerization Pathways'

1

Koval, Michael. "Pathways and control of connexin oligomerization." Trends in Cell Biology 16, no. 3 (March 2006): 159–66. http://dx.doi.org/10.1016/j.tcb.2006.01.006.

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Rhodes, William D., Vladimir I. Kovalchuk, and Mark A. McDonald. "Reaction pathways of halocarbon catalytic oligomerization." Catalysis Communications 18 (February 2012): 98–101. http://dx.doi.org/10.1016/j.catcom.2011.11.019.

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Natarajan, Sudarshan, and Seong H. Kim. "Photochemical oligomerization pathways in 2,5-diiodothiophene film." Journal of Photochemistry and Photobiology A: Chemistry 188, no. 2-3 (May 2007): 342–45. http://dx.doi.org/10.1016/j.jphotochem.2006.12.033.

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Ishizuka, Shinnosuke, Akira Matsugi, Tetsuya Hama, and Shinichi Enami. "Interfacial Water Mediates Oligomerization Pathways of Monoterpene Carbocations." Journal of Physical Chemistry Letters 11, no. 1 (December 6, 2019): 67–74. http://dx.doi.org/10.1021/acs.jpclett.9b03110.

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Kroeger, Karen M., Kevin D. G. Pfleger, and Karin A. Eidne. "G-protein coupled receptor oligomerization in neuroendocrine pathways." Frontiers in Neuroendocrinology 24, no. 4 (December 2003): 254–78. http://dx.doi.org/10.1016/j.yfrne.2003.10.002.

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Lang, Xueting, Tiantian Tang, Tengchuan Jin, Chen Ding, Rongbin Zhou, and Wei Jiang. "TRIM65-catalized ubiquitination is essential for MDA5-mediated antiviral innate immunity." Journal of Experimental Medicine 214, no. 2 (December 28, 2016): 459–73. http://dx.doi.org/10.1084/jem.20160592.

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MDA5 plays a critical role in antiviral innate immunity by functioning as a cytoplasmic double-stranded RNA sensor that can activate type I interferon signaling pathways, but the mechanism for the activation of MDA5 is poorly understood. Here, we show that TRIM65 specifically interacts with MDA5 and promotes K63-linked ubiquitination of MDA5 at lysine 743, which is critical for MDA5 oligomerization and activation. Trim65 deficiency abolishes MDA5 agonist or encephalomyocarditis virus (EMCV)–induced interferon regulatory factor 3 (IRF3) activation and type I interferon production but has no effect on retinoic acid–inducible I (RIG-I), Toll-like receptor 3 (TLR3), or cyclic GMP-AMP synthase signaling pathways. Importantly, Trim65−/− mice are more susceptible to EMCV infection than controls and cannot produce type I interferon in vivo. Collectively, our results identify TRIM65 as an essential component for the MDA5 signaling pathway and provide physiological evidence showing that ubiquitination is important for MDA5 oligomerization and activation.

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Gibson, Luke D., and Jim Pfaendtner. "Solvent oligomerization pathways facilitated by electrolyte additives during solid-electrolyte interphase formation." Physical Chemistry Chemical Physics 22, no. 37 (2020): 21494–503. http://dx.doi.org/10.1039/d0cp03286g.

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Eghiaian, Frederic, Thorsten Daubenfeld, Yann Quenet, Marieke van Audenhaege, Anne-Pascale Bouin, Guillaume van der Rest, Jeanne Grosclaude, and Human Rezaei. "Diversity in prion protein oligomerization pathways results from domain expansion as revealed by hydrogen/deuterium exchange and disulfide linkage." Proceedings of the National Academy of Sciences 104, no. 18 (April 18, 2007): 7414–19. http://dx.doi.org/10.1073/pnas.0607745104.

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The prion protein (PrP) propensity to adopt different structures is a clue to its biological role. PrP oligomers have been previously reported to bear prion infectivity or toxicity and were also found along the pathway of in vitro amyloid formation. In the present report, kinetic and structural analysis of ovine PrP (OvPrP) oligomerization showed that three distinct oligomeric species were formed in parallel, independent kinetic pathways. Only the largest oligomer gave rise to fibrillar structures at high concentration. The refolding of OvPrP into these different oligomers was investigated by analysis of hydrogen/deuterium exchange and introduction of disulfide bonds. These experiments revealed that, before oligomerization, separation of contacts in the globular part (residues 127–234) occurred between the S1–H1–S2 domain (residues 132–167) and the H2–H3 bundle (residues 174–230), implying a conformational change of the S2–H2 loop (residues 168–173). The type of oligomer to be formed depended on the site where the expansion of the OvPrP monomer was initiated. Our data bring a detailed insight into the earlier conformational changes during PrP oligomerization and account for the diversity of oligomeric entities. The kinetic and structural mechanisms proposed here might constitute a physicochemical basis of prion strain genesis.

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Yao, Qiong-Qiong, Jitao Wen, Sarah Perrett, and Si Wu. "Distinct lipid membrane-mediated pathways of Tau assembly revealed by single-molecule analysis." Nanoscale 14, no. 12 (2022): 4604–13. http://dx.doi.org/10.1039/d1nr05960b.

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Single-molecule fluorescence detection reveals the conformational changes and intermolecular oligomerization of microtubule-associated protein Tau induced by DMPS lipid bilayers, and shows distinct assembly pathways depending on lipid concentration.

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Schwantes, Rebecca H., Sophia M. Charan, Kelvin H. Bates, Yuanlong Huang, Tran B. Nguyen, Huajun Mai, Weimeng Kong, Richard C. Flagan, and John H. Seinfeld. "Low-volatility compounds contribute significantly to isoprene secondary organic aerosol (SOA) under high-NO<sub><i>x</i></sub> conditions." Atmospheric Chemistry and Physics 19, no. 11 (June 3, 2019): 7255–78. http://dx.doi.org/10.5194/acp-19-7255-2019.

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Abstract. Recent advances in our knowledge of the gas-phase oxidation of isoprene, the impact of chamber walls on secondary organic aerosol (SOA) mass yields, and aerosol measurement analysis techniques warrant reevaluating SOA yields from isoprene. In particular, SOA from isoprene oxidation under high-NOx conditions forms via two major pathways: (1) low-volatility nitrates and dinitrates (LV pathway) and (2) hydroxymethyl-methyl-α-lactone (HMML) reaction on a surface or the condensed phase of particles to form 2-methyl glyceric acid and its oligomers (2MGA pathway). These SOA production pathways respond differently to reaction conditions. Past chamber experiments generated SOA with varying contributions from these two unique pathways, leading to results that are difficult to interpret. This study examines the SOA yields from these two pathways independently, which improves the interpretation of previous results and provides further understanding of the relevance of chamber SOA yields to the atmosphere and regional or global modeling. Results suggest that low-volatility nitrates and dinitrates produce significantly more aerosol than previously thought; the experimentally measured SOA mass yield from the LV pathway is ∼0.15. Sufficient seed surface area at the start of the reaction is needed to limit the effects of vapor wall losses of low-volatility compounds and accurately measure the complete SOA mass yield. Under dry conditions, substantial amounts of SOA are formed from HMML ring-opening reactions with inorganic ions and HMML organic oligomerization processes. However, the lactone organic oligomerization reactions are suppressed under more atmospherically relevant humidity levels, where hydration of the lactone is more competitive. This limits the SOA formation potential from the 2MGA pathway to HMML ring-opening reactions with water or inorganic ions under typical atmospheric conditions. The isoprene SOA mass yield from the LV pathway measured in this work is significantly higher than previous studies have reported, suggesting that low-volatility compounds such as organic nitrates and dinitrates may contribute to isoprene SOA under high-NOx conditions significantly more than previously thought and thus deserve continued study.

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Coffin, William F., Timothy R. Geiger, and Jennifer M. Martin. "Transmembrane Domains 1 and 2 of the Latent Membrane Protein 1 of Epstein-Barr Virus Contain a Lipid Raft Targeting Signal and Play a Critical Role in Cytostasis." Journal of Virology 77, no. 6 (March 15, 2003): 3749–58. http://dx.doi.org/10.1128/jvi.77.6.3749-3758.2003.

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ABSTRACT The latent membrane protein 1 (LMP-1) oncoprotein of Epstein-Barr virus (EBV) is a constitutively active, CD40-like cell surface signaling protein essential for EBV-mediated human B-cell immortalization. Like ligand-activated CD40, LMP-1 activates NF-κB and Jun kinase signaling pathways via binding, as a constitutive oligomer, to tumor necrosis factor receptor-associated factors (TRAFs). LMP-1's lipid raft association and oligomerization have been linked to its activation of cell signaling pathways. Both oligomerization and lipid raft association require the function of LMP-1's polytopic multispanning transmembrane domain, a domain that is indispensable for LMP-1's growth-regulatory signaling activities. We have begun to address the sequence requirements of the polytopic hydrophobic transmembrane domain for LMP-1's signaling and biochemical activities. Here we report that transmembrane domains 1 and 2 are sufficient for LMP-1's lipid raft association and cytostatic activity. Transmembrane domains 1 and 2 support NF-κB activation, albeit less potently than does the entire polytopic transmembrane domain. Interestingly, LMP-1's first two transmembrane domains are not sufficient for oligomerization or TRAF binding. These results suggest that lipid raft association and oligomerization are mediated by distinct and separable activities of LMP-1's polytopic transmembrane domain. Additionally, lipid raft association, mediated by transmembrane domains 1 and 2, plays a significant role in LMP-1 activation, and LMP-1 can activate NF-κB via an oligomerization/TRAF binding-independent mechanism. To our knowledge, this is the first demonstration of an activity's being linked to individual membrane-spanning domains within LMP-1's polytopic transmembrane domain.

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Koval, Michael. "Differential pathways of claudin oligomerization and integration into tight junctions." Tissue Barriers 1, no. 3 (July 2013): e24518. http://dx.doi.org/10.4161/tisb.24518.

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Renard, P., F. Siekmann, A. Gandolfo, J. Socorro, G. Salque, S. Ravier, E. Quivet, et al. "Radical mechanisms of methyl vinyl ketone oligomerization through aqueous phase OH-oxidation: on the paradoxical role of dissolved molecular oxygen." Atmospheric Chemistry and Physics Discussions 13, no. 1 (January 28, 2013): 2913–54. http://dx.doi.org/10.5194/acpd-13-2913-2013.

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Abstract. It is now accepted that one of the important pathways of Secondary Organic Aerosol (SOA) formation occurs through aqueous phase chemistry in the atmosphere. However, the liquid phase chemical mechanisms leading to macromolecules are still not well understood. For α-dicarbonyl precursors, such as methylglyoxal and glyoxal, radical reactions through OH-oxidation produce oligomers, irreversibly and faster than accretion reactions. Methyl vinyl ketone (MVK) was chosen in the present study as it is an α, β-unsaturated carbonyl that can undergo such reaction pathways in the aqueous phase and forms even high molecular weight oligomers. We present here experiments on the aqueous phase OH-oxidation of MVK, performed under atmospheric relevant conditions. Using NMR and UV absorption spectroscopy, high and ultra-high resolution mass spectrometry, we show that the fast formation of oligomers up to 1800 Da is due to radical oligomerization of MVK, and 13 series of oligomers (out of a total of 26 series) are identified. The influence of atmospherically relevant parameters such as temperature, initial concentrations of MVK and dissolved oxygen are presented and discussed. In agreement with the experimental observations, we propose a chemical mechanism of OH-oxidation of MVK in the aqueous phase that proceeds via radical oligomerization of MVK on the olefin part of the molecule. This mechanism highlights the paradoxical role of dissolved O2: while it inhibits oligomerization reactions, it contributes to produce oligomerization initiator radicals, which rapidly consume O2, thus leading to the supremacy of oligomerization reactions after several minutes of reaction. These processes, together with the large ranges of initial concentrations investigated (60–656 μM of dissolved O2 and 0.2–20 mM of MVK) show the fundamental role that O2 likely plays in atmospheric organic aerosol.

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Ferreira, Cecilia, Silvia Barbosa, Pablo Taboada, Fernando A. Rocha, Ana M. Damas, and Pedro M. Martins. "The nucleation of protein crystals as a race against time with on- and off-pathways." Journal of Applied Crystallography 50, no. 4 (June 30, 2017): 1056–65. http://dx.doi.org/10.1107/s1600576717007312.

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High supersaturation levels are a necessary but insufficient condition for the crystallization of purified proteins. Unlike most small molecules, proteins can take diverse aggregation pathways that make the outcome of crystallization assays quite unpredictable. Here, dynamic light scattering and optical microscopy were used to show that the nucleation of lysozyme crystals is preceded by an initial step of protein oligomerization and by the progressive formation of metastable clusters. Because these steps deplete the concentration of soluble monomers, the probability of obtaining protein crystals decreases as time progresses. Stochastic variations of the induction time are thus amplified to a point where fast crystallization can coexist with unyielding regimes in the same conditions. With an initial hydrodynamic radius of ∼100 nm, the metastable clusters also promote the formation of protein crystals through a mechanism of heterogeneous nucleation. Crystal growth (on-pathway) takes place in parallel with cluster growth (off-pathway). The Janus-faced influence of the mesoscopic clusters is beneficial when it accelerates the formation of the first precrystalline nuclei and is detrimental as it depletes the solution of protein ready to crystallize. Choosing the right balance between the two effects is critical for determining the success of protein crystallization trials. The results presented here suggest that a mild oligomerization degree promotes the formation of a small number of metastable clusters which then catalyze the nucleation of well differentiated crystals.

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Renard, P., F. Siekmann, A. Gandolfo, J. Socorro, G. Salque, S. Ravier, E. Quivet, et al. "Radical mechanisms of methyl vinyl ketone oligomerization through aqueous phase OH-oxidation: on the paradoxical role of dissolved molecular oxygen." Atmospheric Chemistry and Physics 13, no. 13 (July 8, 2013): 6473–91. http://dx.doi.org/10.5194/acp-13-6473-2013.

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Abstract. It is now accepted that one of the important pathways of secondary organic aerosol (SOA) formation occurs through aqueous phase chemistry in the atmosphere. However, the chemical mechanisms leading to macromolecules are still not well understood. It was recently shown that oligomer production by OH radical oxidation in the aerosol aqueous phase from α-dicarbonyl precursors, such as methylglyoxal and glyoxal, is irreversible and fast. Methyl vinyl ketone (MVK) was chosen in the present study as it is an α,β-unsaturated carbonyl that can undergo radical oligomerization in the aerosol aqueous phase. We present here experiments on the aqueous phase OH-oxidation of MVK, performed under various conditions. Using NMR and UV absorption spectroscopy, high and ultra-high resolution mass spectrometry, we show that the fast formation of oligomers up to 1800 Da is due to radical oligomerization of MVK, and 13 series of oligomers (out of a total of 26 series) are identified. The influence of atmospherically relevant parameters such as temperature, initial concentrations of MVK and dissolved oxygen are presented and discussed. In agreement with the experimental observations, we propose a chemical mechanism of OH-oxidation of MVK in the aqueous phase that proceeds via radical oligomerization of MVK on the olefin part of the molecule. This mechanism highlights in our experiments the paradoxical role of dissolved O2: while it inhibits oligomerization reactions, it contributes to produce oligomerization initiator radicals, which rapidly consume O2, thus leading to the dominance of oligomerization reactions after several minutes of reaction. These processes, together with the large range of initial concentrations investigated show the fundamental role that radical oligomerization processes likely play in polluted fogs and atmospheric aerosol.

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Massaccesi, Luca, Emiliano Laudadio, Giovanna Mobbili, Cristina Minnelli, and Roberta Galeazzi. "Cholesterol-mediated oligomerization pathways of serotonin G-coupled receptor 5-HT2C." International Journal of Biological Macromolecules 160 (October 2020): 1090–100. http://dx.doi.org/10.1016/j.ijbiomac.2020.05.231.

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Pun, B. K., and C. Seigneur. "Investigative modeling of new pathways for secondary organic aerosol formation." Atmospheric Chemistry and Physics Discussions 7, no. 1 (January 10, 2007): 203–45. http://dx.doi.org/10.5194/acpd-7-203-2007.

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Abstract. Recent advances in secondary organic aerosol (SOA) research are reviewed and the status of current understanding is investigated using a model of SOA formation. Benzene and isoprene are newly identified precursors that are included in this SOA model; these precursors form SOA via secondary products. The model is also extended to include some representation of aqueous partitioning and the formation of high molecular weight products via oligomerization. Experimental data and empirical relationships are used where possible, because a detailed representation of SOA formation is not supported by the current state of information. Sensitivity studies are conducted with the SOA model and SOA predictions are found to be very sensitive to the treatment of the interactions between particulate water and organic compounds. While uncertainties due to model formulation are significant, influential model parameters include the aerosol partitioning ratios for several small products of isoprene and the partitioning constants for unidentified products (currently, the partitioning constants are derived by fitting experimental data). The pH value used as the reference for the activation of oligomerization is also a critical parameter. Recommendations for future work needed to improve SOA models include the elucidation of the water-organic relationship, the extent of phase separation, and laboratory experiments conducted under conditions more relevant to ambient studies (e.g. lower concentrations, higher relative humidity).

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Pun, B. K., and C. Seigneur. "Investigative modeling of new pathways for secondary organic aerosol formation." Atmospheric Chemistry and Physics 7, no. 9 (May 3, 2007): 2199–216. http://dx.doi.org/10.5194/acp-7-2199-2007.

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Abstract. Recent advances in secondary organic aerosol (SOA) research are reviewed and the status of current understanding is investigated using a box model of SOA formation. Benzene and isoprene are newly identified precursors that are included in this SOA model; these precursors form SOA via secondary products. The model is also extended to include some representation of aqueous partitioning and the formation of high molecular weight products via oligomerization. Experimental data and empirical relationships are used where possible, because a detailed representation of SOA formation is not supported by the current state of information. Sensitivity studies are conducted with the SOA model and SOA predictions are found to be very sensitive to the treatment of the interactions between particulate water and organic compounds. While uncertainties due to model formulation are significant, influential model parameters include the aerosol partitioning ratios for several small products of isoprene and the partitioning constants for unidentified products (currently, the partitioning constants are derived by fitting experimental data). The pH value used as the reference for the activation of oligomerization is also a critical parameter. Recommendations for future work needed to improve SOA models include the elucidation of the water-organic relationship, the extent of phase separation, and laboratory experiments conducted under conditions more relevant to ambient studies (e.g., lower concentrations, higher relative humidity).

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Chadee, Deborah N., Takashi Yuasa, and John M. Kyriakis. "Direct Activation of Mitogen-Activated Protein Kinase Kinase Kinase MEKK1 by the Ste20p Homologue GCK and the Adapter Protein TRAF2." Molecular and Cellular Biology 22, no. 3 (February 1, 2002): 737–49. http://dx.doi.org/10.1128/mcb.22.3.737-749.2002.

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ABSTRACT Mitogen-activated protein kinase (MAPK) pathways coordinate critical cellular responses to mitogens, stresses, and developmental cues. The coupling of MAPK kinase kinase (MAP3K) → MAPK kinase (MEK) → MAPK core pathways to cell surface receptors remains poorly understood. Recombinant forms of MAP3K MEK kinase 1 (MEKK1) interact in vivo and in vitro with the STE20 protein homologue germinal center kinase (GCK), and both GCK and MEKK1 associate in vivo with the adapter protein tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2). These interactions may couple TNF receptors to the SAPK/JNK family of MAPKs; however, a molecular mechanism by which these proteins might collaborate to recruit the SAPKs/JNKs has remained elusive. Here we show that endogenous GCK and MEKK1 associate in vivo. In addition, we have developed an in vitro assay system with which we demonstrate that purified, active GCK and TRAF2 activate MEKK1. The RING domain of TRAF2 is necessary for optimal in vitro activation of MEKK1, but the kinase domain of GCK is not. Autophosphorylation within the MEKK1 kinase domain activation loop is required for activation. Forced oligomerization also activates MEKK1, and GCK elicits enhanced oligomerization of coexpressed MEKK1 in vivo. These results represent the first activation of MEKK1 in vitro using purified proteins and suggest a mechanism for MEKK1 activation involving induced oligomerization and consequent autophosphorylation mediated by upstream proteins.

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Wu, Chuanfeng, Tao Zhen, Guangbiao Zhou, Ping Liu, Zhu Chen, and Saijuan Chen. "Oridonin-Generated Cleavage Fragment of AML1-ETO Inhibits Its Oligomerization and Oncogenic Function Leading to Differentiation and Apoptosis of Leukemic Cells." Blood 114, no. 22 (November 20, 2009): 1051. http://dx.doi.org/10.1182/blood.v114.22.1051.1051.

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Abstract Abstract 1051 Poster Board I-73 Oligomerization through the NHR2 domain is essential for AML1-ETO's inhibition of granulocytic differentiation and enhanced clonogenic potential of primary bone marrow cells. We show here that Oridonin interferes with AML1-ETO oligomerization through its cleavage fragment DAML1-ETO, which consists of the amino acids (aa) 188-752 of the parental oncoprotein or aa 40-604s of the wild-type ETO. DAML1-ETO interacts with the parental AML1-ETO through NHR2 and exerts dominant negative effects on AML1-ETO with regard to DNA binding, transregulatory activity on target genes and regulation of leukemic cell survival, differentiation and proliferation both in vitro and in vivo. Moreover, Oridonin can activate retinoic acid and cAMP/PKA pathways, and potentiate differentiation induced by all-trans retinoic acid (ATRA) and G-CSF. Consistently, combined use of Oridonin, ATRA and G-CSF significantly prolongs lifespan of t (8;21) leukemic mice and, interestingly, we find that this treatment targets the Lin-/Sca-1+/C-KIT+ and Lin-/Sca-1-/C-KIT+ leukemia initiating cells. These data suggest that Oridonin, and potentially other small molecules, can inhibit AML1-ETO oligomerization and leukemogenic function, thus providing a targeted therapy that activates key regulatory pathways for myelomonocytic cell differentiation and apoptosis. Disclosures: No relevant conflicts of interest to declare.

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Wilson, John J., Janelle Grendler, Azaline Dunlap-Smith, Brian F. Beal, and Shallee T. Page. "Analysis of Gene Expression in an Inbred Line of Soft-Shell Clams (Mya arenaria) Displaying Growth Heterosis: Regulation of Structural Genes and the NOD2 Pathway." International Journal of Genomics 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/6720947.

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Mya arenariais a bivalve mollusk of commercial and economic importance, currently impacted by ocean warming, acidification, and invasive species. In order to inform studies on the growth ofM. arenaria, we selected and inbred a population of soft-shell clams for a fast-growth phenotype. This population displayed significantly faster growth (p<0.0001), as measured by 35.4% greater shell size. To assess the biological basis of this growth heterosis, we characterized the complete transcriptomes of six individuals and identified differentially expressed genes by RNAseq. Pathways differentially expressed included structural gene pathways. Also differentially expressed was the nucleotide-binding oligomerization domain 2 (NOD2) receptor pathway that contributes to determination of growth, immunity, apoptosis, and proliferation. NOD2 pathway members that were upregulated included a subset of isoforms ofRIPK2(mean 3.3-fold increase in expression),ERK/MAPK14(3.8-fold),JNK/MAPK8(4.1-fold), andNFκB(4.08-fold). These transcriptomes will be useful resources for both the aquaculture community and researchers with an interest in mollusks and growth heterosis.

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Xu, Xingzhi, Lyuben M. Tsvetkov, and David F. Stern. "Chk2 Activation and Phosphorylation-Dependent Oligomerization." Molecular and Cellular Biology 22, no. 12 (June 15, 2002): 4419–32. http://dx.doi.org/10.1128/mcb.22.12.4419-4432.2002.

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ABSTRACT The tumor suppressor gene CHK2 encodes a versatile effector serine/threonine kinase involved in responses to DNA damage. Chk2 has an amino-terminal SQ/TQ cluster domain (SCD), followed by a forkhead-associated (FHA) domain and a carboxyl-terminal kinase catalytic domain. Mutations in the SCD or FHA domain impair Chk2 checkpoint function. We show here that autophosphorylation of Chk2 produced in a cell-free system requires trans phosphorylation by a wortmannin-sensitive kinase, probably ATM or ATR. Both SQ/TQ sites and non-SQ/TQ sites within the Chk2 SCD can be phosphorylated by active Chk2. Amino acid substitutions in the SCD and the FHA domain impair auto- and trans-kinase activities of Chk2. Chk2 forms oligomers that minimally require the FHA domain of one Chk2 molecule and the SCD within another Chk2 molecule. Chk2 oligomerization in vivo increases after DNA damage, and when damage is induced by gamma irradiation, this increase requires ATM. Chk2 oligomerization is phosphorylation dependent and can occur in the absence of other eukaryotic proteins. Chk2 can cross-phosphorylate another Chk2 molecule in an oligomeric complex. Induced oligomerization of a Chk2 chimera in vivo concomitant with limited DNA damage augments Chk2 kinase activity. These results suggest that Chk2 oligomerization regulates Chk2 activation, signal amplification, and transduction in DNA damage checkpoint pathways.

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Higuchi, Toshio, Takuya Orita, Ken Katsuya, Yoshiki Yamasaki, Kiyotaka Akiyama, Huiping Li, Tadashi Yamamoto, Yutaka Saito, and Motonao Nakamura. "MUC20 Suppresses the Hepatocyte Growth Factor-Induced Grb2-Ras Pathway by Binding to a Multifunctional Docking Site of Met." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7456–68. http://dx.doi.org/10.1128/mcb.24.17.7456-7468.2004.

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ABSTRACT A cDNA encoding a novel mucin protein, MUC20, was isolated as a gene that is up-regulated in the renal tissues of patients with immunoglobulin A nephropathy. We demonstrate here that the C terminus of MUC20 associates with the multifunctional docking site of Met without ligand activation, preventing Grb2 recruitment to Met and thus attenuating hepatocyte growth factor (HGF)-induced transient extracellular signal-regulated kinase-1 and -2 activation. Production of MUC20 reduced HGF-induced matrix metalloproteinase expression and proliferation, which require the Grb2-Ras pathway, whereas cell scattering, branching morphogenesis, and survival via the Gab1/phosphatidylinositol 3-kinase (PI3K) pathways was not affected. Thus, MUC20 reduces HGF-induced activation of the Grb2-Ras pathway but not the Gab1/PI3K pathways. We further demonstrate that the cytoplasmic domain of MUC20 has the ability to oligomerize and that the oligomerization augments its affinity for Met. Taken together, these results suggest that MUC20 is a novel regulator of the Met signaling cascade which has a role in suppression of the Grb2-Ras pathway.

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Matthes, Dirk, Vytautas Gapsys, Venita Daebel, and Bert L. de Groot. "Mapping the Conformational Dynamics and Pathways of Spontaneous Steric Zipper Peptide Oligomerization." PLoS ONE 6, no. 5 (May 3, 2011): e19129. http://dx.doi.org/10.1371/journal.pone.0019129.

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Clark, Janet R., Phillip E. Fanwick, and Ian P. Rothwell. "Reaction pathways for the oligomerization of organic isocyanides by tantalum hydride reagents." Journal of the Chemical Society, Chemical Communications, no. 15 (1993): 1233. http://dx.doi.org/10.1039/c39930001233.

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Wang, Quan, Andrew J. Serban, Rebekka M. Wachter, and W. E. Moerner. "Single-molecule diffusometry reveals the nucleotide-dependent oligomerization pathways ofNicotiana tabacumRubisco activase." Journal of Chemical Physics 148, no. 12 (March 28, 2018): 123319. http://dx.doi.org/10.1063/1.5005930.

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Phelps, Erin M., and Carol K. Hall. "Structural transitions and oligomerization along polyalanine fibril formation pathways from computer simulations." Proteins: Structure, Function, and Bioinformatics 80, no. 6 (March 13, 2012): 1582–97. http://dx.doi.org/10.1002/prot.24052.

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Klein, J. C. Von Vaupel. "OLIGOMERIZATION IN COPEPODA CYCLOPOIDA AS A KIND OF ORTHOGENETIC EVOLUTION IN THE ANIMAL KINGDOM." Crustaceana 72, no. 3 (1999): 241–64. http://dx.doi.org/10.1163/156854099503320.

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AbstractThe morphological-evolutionary notions on oligomerization (i.e., reduction in numbers of segments) of the thoracic limbs and the first antenna in Copepoda Cyclopoida are examined in detail. It is shown that the process of oligomerization is correlated to a large extent with a decrease in body length. The oligomerization of the thoracic limbs is evolutionarily irreversible, thus capable of channeling the further pathways of morphological development. Consequently, its successive steps in phylogenetic lineages are considered to represent a kind of orthogenetic evolution. Les notions morphologiques-evolutionnaires sur l'oligomerisation (c'est-a-dire sur la reduction du nombre des segments) des pattes thoraciques et de la premiere antenne chez les Copepodes Cyclopoida sont examinees en detail. Il est montre que le processus d'oligomerisation est en correlation dans une large mesure avec une diminution de la longueur du corps. L'oligomerisation des pattes thoraciques est evolutionnairement irreversible, etant ainsi capable d'orienter le cours ulterieur du developpement morphologique. Par consequent, ses pas successifs dans les lignees phylogenetiques sont consideres comme representant une sorte d'evolution orthogenetique.

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Darsow, Tamara, David J. Katzmann, Christopher R. Cowles, and Scott D. Emr. "Vps41p Function in the Alkaline Phosphatase Pathway Requires Homo-oligomerization and Interaction with AP-3 through Two Distinct Domains." Molecular Biology of the Cell 12, no. 1 (January 2001): 37–51. http://dx.doi.org/10.1091/mbc.12.1.37.

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Transport of proteins through the ALP (alkaline phosphatase) pathway to the vacuole requires the function of the AP-3 adaptor complex and Vps41p. However, unlike other adaptor protein–dependent pathways, the ALP pathway has not been shown to require additional accessory proteins or coat proteins, such as membrane recruitment factors or clathrin. Two independent genetic approaches have been used to identify new mutants that affect transport through the ALP pathway. These screens yielded new mutants in both VPS41 and the four AP-3 subunit genes. Two new VPS41 alleles exhibited phenotypes distinct from null mutants of VPS41, which are defective in vacuolar morphology and protein transport through both the ALP and CPY sorting pathways. The new alleles displayed severe ALP sorting defects, normal vacuolar morphology, and defects in ALP vesicle formation at the Golgi complex. Sequencing analysis of theseVPS41 alleles revealed mutations encoding amino acid changes in two distinct domains of Vps41p: a conserved N-terminal domain and a C-terminal clathrin heavy-chain repeat (CHCR) domain. We demonstrate that the N-terminus of Vps41p is required for binding to AP-3, whereas the C-terminal CHCR domain directs homo-oligomerization of Vps41p. These data indicate that a homo-oligomeric form of Vps41p is required for the formation of ALP containing vesicles at the Golgi complex via interactions with AP-3.

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Zhou, Tao, Zhihua Fang, Daniel F. C. Duarte, Stefan A. Fernandes, Ying Lu, Jing Guo, Lang Gui, and Liangbiao Chen. "Transcriptome Analysis of Immune Response against Streptococcus agalactiae Infection in the Nile Tilapia GIFT Strain." Fishes 7, no. 5 (September 20, 2022): 246. http://dx.doi.org/10.3390/fishes7050246.

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Streptococcus agalactiae (group B streptococcus, GBS), a broad-spectrum pathogen, causes great economic losses in fish aquaculture, especially the industry of tilapia. Until now, the knowledge of the immune response mechanism against S. agalactiae infection in tilapia has been limited. In the present study, the gill transcriptome of the tilapia from the GBS and the phosphate buffered saline (PBS) groups were sequenced. The transcriptomic analysis results presented the differentially expressed genes (DEGs) at different time points (DEGs number, 6 h: 2122, 9 h: 1851, 15 h: 1791, and 18 h: 2395) after GBS injection, and significantly enriched immune-related gene ontology (GO) terms such as the innate immune response. The significantly enriched immune pathways included the Toll-like receptor signaling pathway, the nucleotide oligomerization domain (NOD)-like receptor signaling pathway, the cytosolic-DNA sensing pathway, and the intestinal immune network for Immunoglobulin A (IgA) production. Most of the DEGs in Toll-like receptor signaling, NOD-like receptor signaling, and cytosolic-DNA sensing pathways presented upregulations at 18 h, which indicated that the innate immune pathways were activated. Two immune-related pathways (phagosome and cell adhesion molecules) were significantly enriched at all time points, suggesting that these two pathways might also play important roles in the immune response against the GBS infection. The results of HE staining showed that the gills of tilapia were damaged seriously at 9 h post-infection, which might be due to the possibility of pyroptosis resulting from the changes of DEGs in the NOD-like receptor signaling pathway. This study provided new insight into the mechanisms of gill damage in fish infected with S. agalactiae.

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Kua, Jeremy, and Helen Loli. "Porphinogen Formation from the Co-Oligomerization of Formaldehyde and Pyrrole: Free Energy Pathways." Journal of Physical Chemistry A 121, no. 42 (October 13, 2017): 8154–65. http://dx.doi.org/10.1021/acs.jpca.7b08685.

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Strasser, Jürgen, Rob N. de Jong, Frank J. Beurskens, Guanbo Wang, Albert J. R. Heck, Janine Schuurman, Paul W. H. I. Parren, Peter Hinterdorfer, and Johannes Preiner. "Unraveling the Macromolecular Pathways of IgG Oligomerization and Complement Activation on Antigenic Surfaces." Nano Letters 19, no. 7 (June 6, 2019): 4787–96. http://dx.doi.org/10.1021/acs.nanolett.9b02220.

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Vaidyanathan, M. S., Pradeep Sathyanarayana, Prabal K. Maiti, Sandhya S. Visweswariah, and K. G. Ayappa. "Lysis dynamics and membrane oligomerization pathways for Cytolysin A (ClyA) pore-forming toxin." RSC Advances 4, no. 10 (2014): 4930. http://dx.doi.org/10.1039/c3ra45159c.

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Jafari, Naeimeh, Jason Del Rio, Madoka Akimoto, Jung Ah Byun, Stephen Boulton, Kody Moleschi, Yousif Alsayyed, et al. "Noncanonical protein kinase A activation by oligomerization of regulatory subunits as revealed by inherited Carney complex mutations." Proceedings of the National Academy of Sciences 118, no. 21 (May 18, 2021): e2024716118. http://dx.doi.org/10.1073/pnas.2024716118.

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Familial mutations of the protein kinase A (PKA) R1α regulatory subunit lead to a generalized predisposition for a wide range of tumors, from pituitary adenomas to pancreatic and liver cancers, commonly referred to as Carney complex (CNC). CNC mutations are known to cause overactivation of PKA, but the molecular mechanisms underlying such kinase overactivity are not fully understood in the context of the canonical cAMP-dependent activation of PKA. Here, we show that oligomerization-induced sequestration of R1α from the catalytic subunit of PKA (C) is a viable mechanism of PKA activation that can explain the CNC phenotype. Our investigations focus on comparative analyses at the level of structure, unfolding, aggregation, and kinase inhibition profiles of wild-type (wt) PKA R1α, the A211D and G287W CNC mutants, as well as the cognate acrodysostosis type 1 (ACRDYS1) mutations A211T and G287E. The latter exhibit a phenotype opposite to CNC with suboptimal PKA activation compared with wt. Overall, our results show that CNC mutations not only perturb the classical cAMP-dependent allosteric activation pathway of PKA, but also amplify significantly more than the cognate ACRDYS1 mutations nonclassical and previously unappreciated activation pathways, such as oligomerization-induced losses of the PKA R1α inhibitory function.

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Belkin, Alexey M., Galina Tsurupa, Evgeny Zemskov, Yuri Veklich, John W. Weisel, and Leonid Medved. "Transglutaminase-mediated oligomerization of the fibrin(ogen) αC domains promotes integrin-dependent cell adhesion and signaling." Blood 105, no. 9 (May 1, 2005): 3561–68. http://dx.doi.org/10.1182/blood-2004-10-4089.

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AbstractInteractions of endothelial cells with fibrin(ogen) are implicated in inflammation, angiogenesis, and wound healing. Cross-linking of the fibrinogen αC domains with factor XIIIa generates ordered αC oligomers mimicking polymeric arrangement of the αC domains in fibrin. These oligomers and those prepared with tissue transglutaminase were used to establish a mechanism of the αC domain–mediated interaction of fibrin with endothelial cells. Cell adhesion and chemical cross-linking experiments revealed that oligomerization of the αC domains by both transglutaminases significantly increases their RGD (arginyl–glycyl–aspartate)–dependent interaction with endothelial αVβ3 and to a lesser extent with αVβ5 and α5β1 integrins. The oligomerization promotes integrin clustering, thereby increasing cell adhesion, spreading, formation of prominent peripheral focal contacts, and integrin-mediated activation of focal adhesion kinase (FAK) and extracellular signal-regulated kinase (ERK) signaling pathways. The enhanced integrin clustering is likely caused by ordered juxtaposition of RGD-containing integrin-binding sites upon oligomerization of the αC domains and increased affinity of these domains for integrins. Our findings provide new insights into the mechanism of the αC domain–mediated interaction of endothelial cells with fibrin and imply its potential involvement in cell migration. They also suggest a new role for transglutaminases in regulation of integrin-mediated adhesion and signaling via covalent modification of integrin ligands.

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Petrone, A., and J. Sap. "Emerging issues in receptor protein tyrosine phosphatase function: lifting fog or simply shifting?" Journal of Cell Science 113, no. 13 (July 1, 2000): 2345–54. http://dx.doi.org/10.1242/jcs.113.13.2345.

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Transmembrane (receptor) tyrosine phosphatases are intimately involved in responses to cell-cell and cell-matrix contact. Several important issues regarding the targets and regulation of this protein family are now emerging. For example, these phosphatases exhibit complex interactions with signaling pathways involving SRC family kinases, which result from their ability to control phosphorylation of both activating and inhibitory sites in these kinases and possibly also their substrates. Similarly, integrin signaling illustrates how phosphorylation of a single protein, or the activity of a pathway, can be controlled by multiple tyrosine phosphatases, attesting to the intricate integration of these enzymes in cellular regulation. Lastly, we are starting to appreciate the roles of intracellular topology, tyrosine phosphorylation and oligomerization among the many mechanisms regulating tyrosine phosphatase activity.

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Nazarian-Samani, Zeinab, Robert D. E. Sewell, and Mahmoud Rafieian-Kopaei. "Inflammasome Signaling and Other Factors Implicated in Atherosclerosis Development and Progression." Current Pharmaceutical Design 26, no. 22 (July 5, 2020): 2583–90. http://dx.doi.org/10.2174/1381612826666200504115045.

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Chronic inflammation plays an extensive role in the onset and progression of metabolic disorders such as atherosclerosis, type 2 diabetes, gout and obesity. Atherosclerosis accounts for up to 70% mortality in patients with type 2 diabetes and is also a chronic condition that causes atrial stenosis due to a lipometabolism imbalance. The purpose of this article is to consider the inflammatory factors implicated in atherosclerosis and their role in the development and progression of this vascular disease. The inflammasome signaling pathway is an important inflammatory mechanism involved in the development of atherosclerosis. The most important inflammasome pathway in this respect is the NLRP3 inflammasome (Nucleotide-binding oligomerization domain (NOD)-like receptor with a pyrin domain 3), whose activation leads to the generation of important inflammatory cytokines including interleukins 1β and 18 (IL-1β and 18). The activities of these mature cytokines and inflammatory factors produced by other inflammatory pathways lead to arterial inflammation and eventually arterial occlusion, which can result in life-threatening complications such as myocardial infarction and stroke. Therefore, it is essential to seek out more precise mechanisms for the activation of inflammasomes and other inflammatory pathways for the development of therapeutic strategies of atherosclerosis.

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van der Graaf, Chantal A. A., Mihai G. Netea, Barbara Franke, Stephen E. Girardin, Jos W. M. van der Meer, and Bart Jan Kullberg. "Nucleotide Oligomerization Domain 2 (Nod2) Is Not Involved in the Pattern Recognition of Candida albicans." Clinical and Vaccine Immunology 13, no. 3 (March 2006): 423–25. http://dx.doi.org/10.1128/cvi.13.3.423-425.2006.

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ABSTRACT Nucleotide-binding oligomerization domain 2 (Nod2) pathways are known to interact with Toll-like receptor 2 (TLR2) and TLR4, which are pattern recognition receptors for Candida albicans. We observed that the prevalence of Nod2 polymorphisms was not increased in patients with Candida infections. Candida-induced cytokine production in individuals with Nod2 polymorphisms was unaffected. We conclude that Nod2 is unlikely to play an important role in the recognition of Candida albicans.

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Madahar, Vipul, Runrui Dang, Quanqing Zhang, Chuchu Liu, Victor G. J. Rodgers, and Jiayu Liao. "Human Post-Translational SUMOylation Modification of SARS-CoV-2 Nucleocapsid Protein Enhances Its Interaction Affinity with Itself and Plays a Critical Role in Its Nuclear Translocation." Viruses 15, no. 7 (July 21, 2023): 1600. http://dx.doi.org/10.3390/v15071600.

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Viruses, such as Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), infect hosts and take advantage of host cellular machinery for genome replication and new virion production. Identifying and elucidating host pathways for viral infection is critical for understanding the development of the viral life cycle and novel therapeutics. The SARS-CoV-2 N protein is critical for viral RNA (vRNA) genome packaging in new virion formation. Using our quantitative Förster energy transfer/Mass spectrometry (qFRET/MS) coupled method and immunofluorescence imaging, we identified three SUMOylation sites of the SARS-CoV-2 N protein. We found that (1) Small Ubiquitin-like modifier (SUMO) modification in Nucleocapsid (N) protein interaction affinity increased, leading to enhanced oligomerization of the N protein; (2) one of the identified SUMOylation sites, K65, is critical for its nuclear translocation. These results suggest that the host human SUMOylation pathway may be critical for N protein functions in viral replication and pathology in vivo. Thus, blocking essential host pathways could provide a novel strategy for future anti-viral therapeutics development, such as for SARS-CoV-2 and other viruses.

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Harkness, Robert W., Yuki Toyama, Zev A. Ripstein, Huaying Zhao, Alexander I. M. Sever, Qing Luan, Jacob P. Brady, Patricia L. Clark, Peter Schuck, and Lewis E. Kay. "Competing stress-dependent oligomerization pathways regulate self-assembly of the periplasmic protease-chaperone DegP." Proceedings of the National Academy of Sciences 118, no. 32 (August 6, 2021): e2109732118. http://dx.doi.org/10.1073/pnas.2109732118.

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DegP is an oligomeric protein with dual protease and chaperone activity that regulates protein homeostasis and virulence factor trafficking in the periplasm of gram-negative bacteria. A number of oligomeric architectures adopted by DegP are thought to facilitate its function. For example, DegP can form a “resting” hexamer when not engaged to substrates, mitigating undesired proteolysis of cellular proteins. When bound to substrate proteins or lipid membranes, DegP has been shown to populate a variety of cage- or bowl-like oligomeric states that have increased proteolytic activity. Though a number of DegP’s substrate-engaged structures have been robustly characterized, detailed mechanistic information underpinning its remarkable oligomeric plasticity and the corresponding interplay between these dynamics and biological function has remained elusive. Here, we have used a combination of hydrodynamics and NMR spectroscopy methodologies in combination with cryogenic electron microscopy to shed light on the apo-DegP self-assembly mechanism. We find that, in the absence of bound substrates, DegP populates an ensemble of oligomeric states, mediated by self-assembly of trimers, that are distinct from those observed in the presence of substrate. The oligomeric distribution is sensitive to solution ionic strength and temperature and is shifted toward larger oligomeric assemblies under physiological conditions. Substrate proteins may guide DegP toward canonical cage-like structures by binding to these preorganized oligomers, leading to changes in conformation. The properties of DegP self-assembly identified here suggest that apo-DegP can rapidly shift its oligomeric distribution in order to respond to a variety of biological insults.

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Trimm, David L., Irene O. Y. Liu, and Noel W. Cant. "The oligomerization of acetylene in hydrogen over Ni/SiO2 catalysts: Product distribution and pathways." Journal of Molecular Catalysis A: Chemical 288, no. 1-2 (June 2008): 63–74. http://dx.doi.org/10.1016/j.molcata.2008.03.022.

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Fang, Guibin, Yuan Fu, Shixun Li, Junxiong Qiu, Manyuan Kuang, Sipeng Lin, Changchuan Li, and Yue Ding. "The USP14–NLRC5 pathway inhibits titanium particle–induced osteolysis in mice by suppressing NF-κB and PI3K/AKT activities." Journal of Biological Chemistry 295, no. 20 (April 9, 2020): 7018–32. http://dx.doi.org/10.1074/jbc.ra119.012495.

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Total hip arthroplasty (THA) is a widely-used surgical intervention for treating patients with end-stage degenerative and inflammatory osteoarthropathy. However, wear particles from the artificial titanium joint can induce osteolysis, limiting the long-term survivorship of THA. Monocyte/macrophage lineage cells are the key players in the response to wear particles, and the proinflammatory NF-κB and phosphoinositide 3-kinase (PI3K)–AKT Ser/Thr kinase (AKT)-signaling pathways have been shown to be the most important contributors to wear particle–induced osteolysis. In contrast, ubiquitin-specific protease 14 (USP14) specifically removes the polyubiquitin chains from the nucleotide-binding and oligomerization domain (NOD)-like receptor family Caspase recruitment domain (CARD)–containing 5 (NLRC5) and thereby enhances the NLRC5-mediated inhibition of NF-κB signaling. In this study, we aimed to clarify the role of the USP14–NLRC5 pathway in wear particle–induced osteolysis in vitro and in vivo. We found that NLRC5 or USP14 overexpression inhibits titanium particle–induced proinflammatory tumor necrosis factor α (TNFα) production and NF-κB pathway activation, and it also decreases M1 macrophage polarization and PI3K/AKT pathway activation. Of note, NLRC5 and USP14 overexpression attenuated titanium particle–induced cranial osteolysis in mice. In conclusion, the findings of our study indicate that the USP14–NLRC5 pathway inhibits titanium particle–induced osteolysis by suppressing the NF-κB and PI3K/AKT pathways both in vitro and in vivo.

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Martínez-Carranza, Markel, Venkateswara Rao Jonna, Daniel Lundin, Margareta Sahlin, Lars-Anders Carlson, Newal Jemal, Martin Högbom, Britt-Marie Sjöberg, Pål Stenmark, and Anders Hofer. "A ribonucleotide reductase from Clostridium botulinum reveals distinct evolutionary pathways to regulation via the overall activity site." Journal of Biological Chemistry 295, no. 46 (September 3, 2020): 15576–87. http://dx.doi.org/10.1074/jbc.ra120.014895.

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Ribonucleotide reductase (RNR) is a central enzyme for the synthesis of DNA building blocks. Most aerobic organisms, including nearly all eukaryotes, have class I RNRs consisting of R1 and R2 subunits. The catalytic R1 subunit contains an overall activity site that can allosterically turn the enzyme on or off by the binding of ATP or dATP, respectively. The mechanism behind the ability to turn the enzyme off via the R1 subunit involves the formation of different types of R1 oligomers in most studied species and R1–R2 octamers in Escherichia coli. To better understand the distribution of different oligomerization mechanisms, we characterized the enzyme from Clostridium botulinum, which belongs to a subclass of class I RNRs not studied before. The recombinantly expressed enzyme was analyzed by size-exclusion chromatography, gas-phase electrophoretic mobility macromolecular analysis, EM, X-ray crystallography, and enzyme assays. Interestingly, it shares the ability of the E. coli RNR to form inhibited R1–R2 octamers in the presence of dATP but, unlike the E. coli enzyme, cannot be turned off by combinations of ATP and dGTP/dTTP. A phylogenetic analysis of class I RNRs suggests that activity regulation is not ancestral but was gained after the first subclasses diverged and that RNR subclasses with inhibition mechanisms involving R1 oligomerization belong to a clade separated from the two subclasses forming R1–R2 octamers. These results give further insight into activity regulation in class I RNRs as an evolutionarily dynamic process.

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Renard, P., F. Siekmann, G. Salque, A. Smaani, C. Demelas, B. Coulomb, L. Vassalo, et al. "Aqueous phase oligomerization of methyl vinyl ketone through photooxidation – Part 1: Aging processes of oligomers." Atmospheric Chemistry and Physics Discussions 14, no. 10 (June 12, 2014): 15283–322. http://dx.doi.org/10.5194/acpd-14-15283-2014.

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Abstract. Secondary organic aerosol (SOA) represents a substantial part of organic aerosol, which affects climate and human health. It is now accepted that one of the important pathways of SOA formation occurs via aqueous phase chemistry in the atmosphere. Recently, we have shown in a previous study (Renard et al., 2013) the mechanism of oligomerization of MVK (methyl vinyl ketone), and suggested that unsaturated water soluble organic compounds (UWSOC) might efficiently form SOA in wet aerosol particles, even for weakly soluble ones like MVK. The atmospheric relevance of these processes is explored by means of process model studies (in a companion paper). In the present study we investigate the aging of these aqueous phase MVK-oligomers (Part 1). We compared aqueous phase composition and SOA composition after nebulization, mainly by means of UPLC-ESI-MS and AMS, respectively. Both instruments match and show similar trend of oligomer formation and aging. The SMPS analysis performed on the nebulized solutions allow to quantify these SOA and to measure their mass yields. We have highlighted in the current study that MVK •OH-oxidation undergoes kinetic competition between functionalization and oligomerization. The SOA composition and its evolution highly depend on the precursor initial concentration. We determined the threshold of MVK concentration, i.e. 2 mM, from which oligomerization prevails over functionalization. Hence, at these concentrations, •OH-oxidation of MVK forms oligomers that are SV-OOA, with low O / C and high f43. Oligomers are then fragmented, via unidentified intermediates that have the properties of LV-OOA which then end into succinic, malonic and oxalic diacids. For lower initial MVK concentrations, the oligomerization is not the major process, and functionalization dominates, resulting in small carbonyls, dicarbonyls and mainly monoacids. The aging of these oligomers could be an explanation for the presence of a part of the diacids observed in aerosol.

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Lattanzi, Roberta, and Rossella Miele. "Prokineticin-Receptor Network: Mechanisms of Regulation." Life 12, no. 2 (January 25, 2022): 172. http://dx.doi.org/10.3390/life12020172.

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Prokineticins are a new class of chemokine-like peptides that bind their G protein-coupled receptors, PKR1 and PKR2, and promote chemotaxis and the production of pro-inflammatory cytokines following tissue injury or infection. This review summarizes the major cellular and biochemical mechanisms of prokineticins pathway regulation that, like other chemokines, include: genetic polymorphisms; mRNA splice modulation; expression regulation at transcriptional and post-transcriptional levels; prokineticins interactions with cell-surface glycosaminoglycans; PKRs degradation, localization, post-translational modifications and oligomerization; alternative signaling responses; binding to pharmacological inhibitors. Understanding these mechanisms, which together exert substantial biochemical control and greatly enhance the complexity of the prokineticin-receptor network, leads to novel opportunities for therapeutic intervention. In this way, besides targeting prokineticins or their receptors directly, it could be possible to indirectly influence their activity by modulating their expression and localization or blocking the downstream signaling pathways.

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Perica, Tina, Yasushi Kondo, Sandhya P. Tiwari, Stephen H. McLaughlin, Katherine R. Kemplen, Xiuwei Zhang, Annette Steward, Nathalie Reuter, Jane Clarke, and Sarah A. Teichmann. "Evolution of oligomeric state through allosteric pathways that mimic ligand binding." Science 346, no. 6216 (December 18, 2014): 1254346. http://dx.doi.org/10.1126/science.1254346.

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Evolution and design of protein complexes are almost always viewed through the lens of amino acid mutations at protein interfaces. We showed previously that residues not involved in the physical interaction between proteins make important contributions to oligomerization by acting indirectly or allosterically. In this work, we sought to investigate the mechanism by which allosteric mutations act, using the example of the PyrR family of pyrimidine operon attenuators. In this family, a perfectly sequence-conserved helix that forms a tetrameric interface is exposed as solvent-accessible surface in dimeric orthologs. This means that mutations must be acting from a distance to destabilize the interface. We identified 11 key mutations controlling oligomeric state, all distant from the interfaces and outside ligand-binding pockets. Finally, we show that the key mutations introduce conformational changes equivalent to the conformational shift between the free versus nucleotide-bound conformations of the proteins.

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Zhang, W., N. Liu, X. Wang, X. Jin, H. Du, G. Peng, and J. Xue. "Benzo(a)pyrene-7,8-diol-9,10-epoxide induced p53-independent necrosis via the mitochondria-associated pathway involving Bax and Bak activation." Human & Experimental Toxicology 34, no. 2 (May 16, 2014): 179–90. http://dx.doi.org/10.1177/0960327114533358.

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Benzo(a)pyrene-7,8-diol-9,10-epoxide (BPDE) is a highly reactive DNA damage agent and can induce cell death through both p53-independent and -dependent pathways. However, little is known about the molecular mechanisms of p53-independent pathways in BPDE-induced cell death. To understand the p53-independent mechanisms, we have now examined BPDE-induced cytotoxicity in p53-deficient baby mouse kidney (BMK) cells. The results showed that BPDE could induce Bax and Bak activation, cytochrome c release, caspases activation, and necrotic cell death in the BMK cells. Bax and Bak, two key molecules of mitochondrial permeability transition pore, were interdependently activated by BPDE, with Bax and Bak translocation to and Bax/Bak homo-oligomerization in mitochondria, release of cytochrome c was induced. Importantly, cytochrome c release and necrotic cell death were diminished in BMK cells (Bax−/−), BMK cells (Bak−/−), and BMK cells (Bax−/−/Bak−/−). Furthermore, overexpression of Bcl-2 could ameliorate BPDE-induced cytochrome c release and necrosis. Together the findings suggested that BPDE-induced necrosis was modulated by the p53-independent pathway, which was related to the translocation of Bax and Bak to mitochondria, release of cytochrome c, and activation of caspases.

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Franco, María Luisa, Irmina García-Carpio, Raquel Comaposada-Baró, Juan J. Escribano-Saiz, Lucía Chávez-Gutiérrez, and Marçal Vilar. "TrkA-mediated endocytosis of p75-CTF prevents cholinergic neuron death upon γ-secretase inhibition." Life Science Alliance 4, no. 4 (February 3, 2021): e202000844. http://dx.doi.org/10.26508/lsa.202000844.

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γ-secretase inhibitors (GSI) were developed to reduce the generation of Aβ peptide to find new Alzheimer’s disease treatments. Clinical trials on Alzheimer’s disease patients, however, showed several side effects that worsened the cognitive symptoms of the treated patients. The observed side effects were partially attributed to Notch signaling. However, the effect on other γ-secretase substrates, such as the p75 neurotrophin receptor (p75NTR) has not been studied in detail. p75NTR is highly expressed in the basal forebrain cholinergic neurons (BFCNs) during all life. Here, we show that GSI treatment induces the oligomerization of p75CTF leading to the cell death of BFCNs, and that this event is dependent on TrkA activity. The oligomerization of p75CTF requires an intact cholesterol recognition sequence (CRAC) and the constitutive binding of TRAF6, which activates the JNK and p38 pathways. Remarkably, TrkA rescues from cell death by a mechanism involving the endocytosis of p75CTF. These results suggest that the inhibition of γ-secretase activity in aged patients, where the expression of TrkA in the BFCNs is already reduced, could accelerate cholinergic dysfunction and promote neurodegeneration.

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Holler, Nils, Aubry Tardivel, Magdalena Kovacsovics-Bankowski, Sylvie Hertig, Olivier Gaide, Fabio Martinon, Antoine Tinel, et al. "Two Adjacent Trimeric Fas Ligands Are Required for Fas Signaling and Formation of a Death-Inducing Signaling Complex." Molecular and Cellular Biology 23, no. 4 (February 15, 2003): 1428–40. http://dx.doi.org/10.1128/mcb.23.4.1428-1440.2003.

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ABSTRACT The membrane-bound form of Fas ligand (FasL) signals apoptosis in target cells through engagement of the death receptor Fas, whereas the proteolytically processed, soluble form of FasL does not induce cell death. However, soluble FasL can be rendered active upon cross-linking. Since the minimal extent of oligomerization of FasL that exerts cytotoxicity is unknown, we engineered hexameric proteins containing two trimers of FasL within the same molecule. This was achieved by fusing FasL to the Fc portion of immunoglobulin G1 or to the collagen domain of ACRP30/adiponectin. Trimeric FasL and hexameric FasL both bound to Fas, but only the hexameric forms were highly cytotoxic and competent to signal apoptosis via formation of a death-inducing signaling complex. Three sequential early events in Fas-mediated apoptosis could be dissected, namely, receptor binding, receptor activation, and recruitment of intracellular signaling molecules, each of which occurred independently of the subsequent one. These results demonstrate that the limited oligomerization of FasL, and most likely of some other tumor necrosis factor family ligands such as CD40L, is required for triggering of the signaling pathways.

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Steffen, Janos, Ajay A. Vashisht, Jijun Wan, Joanna C. Jen, Steven M. Claypool, James A. Wohlschlegel, and Carla M. Koehler. "Rapid degradation of mutant SLC25A46 by the ubiquitin-proteasome system results in MFN1/2-mediated hyperfusion of mitochondria." Molecular Biology of the Cell 28, no. 5 (March 2017): 600–612. http://dx.doi.org/10.1091/mbc.e16-07-0545.

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SCL25A46 is a mitochondrial carrier protein that surprisingly localizes to the outer membrane and is distantly related to Ugo1. Here we show that a subset of SLC25A46 interacts with mitochondrial dynamics components and the MICOS complex. Decreased expression of SLC25A46 results in increased stability and oligomerization of MFN1 and MFN2 on mitochondria, promoting mitochondrial hyperfusion. A mutation at L341P causes rapid degradation of SLC25A46, which manifests as a rare disease, pontocerebellar hypoplasia. The E3 ubiquitin ligases MULAN and MARCH5 coordinate ubiquitylation of SLC25A46 L341P, leading to degradation by organized activities of P97 and the proteasome. Whereas outer mitochondrial membrane–associated degradation is typically associated with apoptosis or a specialized type of autophagy termed mitophagy, SLC25A46 degradation operates independently of activation of outer membrane stress pathways. Thus SLC25A46 is a new component in mitochondrial dynamics that serves as a regulator for MFN1/2 oligomerization. Moreover, SLC25A46 is selectively degraded from the outer membrane independently of mitophagy and apoptosis, providing a framework for mechanistic studies in the proteolysis of outer membrane proteins.

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Journal articles on the topic 'Oligomerization Pathways'

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