Advances in biological regulation最新文献

{"title":"Sphingolipids and their role in health and disease in the central nervous system","authors":"Andrés Felipe Leal ,&nbsp;Diego A. Suarez ,&nbsp;Olga Yaneth Echeverri-Peña ,&nbsp;Sonia Luz Albarracín ,&nbsp;Carlos Javier Alméciga-Díaz ,&nbsp;Ángela Johana Espejo-Mojica","doi":"10.1016/j.jbior.2022.100900","DOIUrl":"10.1016/j.jbior.2022.100900","url":null,"abstract":"<div><p><span>Sphingolipids<span> (SLs) are lipids<span> derived from sphingosine, and their metabolism involves a broad and complex network of reactions. Although SLs are widely distributed in the body, it is well known that they are present in high concentrations within the central nervous system (CNS). Under physiological conditions, their abundance and distribution in the CNS depend on brain development and cell type. Consequently, </span></span></span>SLs metabolism<span><span> impairment may have a significant impact on the normal CNS function, and has been associated with several disorders, including </span>sphingolipidoses, Parkinson's, and Alzheimer's. This review summarizes the main SLs characteristics and current knowledge about synthesis, catabolism, regulatory pathways, and their role in physiological and pathological scenarios in the CNS.</span></p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"85 ","pages":"Article 100900"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10739546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphoregulation of the ATP synthase beta subunit stimulates mitochondrial activity for G2/M progression","authors":"Ana Cláudia Leite ,&nbsp;Telma Silva Martins ,&nbsp;Ana Campos ,&nbsp;Vítor Costa ,&nbsp;Clara Pereira","doi":"10.1016/j.jbior.2022.100905","DOIUrl":"10.1016/j.jbior.2022.100905","url":null,"abstract":"<div><p><span><span><span>Mitochondrial ATP synthase is a multifunctional </span>enzyme complex involved in ATP production. We previously reported that the ATP synthase catalytic </span>beta subunit (Atp2p in yeast) is regulated by the 2A-like </span>protein phosphatase<span> Sit4p, which targets Atp2p at T124/T317 impacting on ATP synthase levels and mitochondrial respiration.</span></p><p><span>Here we report that Atp2-T124/T317 is also potentially regulated by Cdc5p, a polo-like mitotic kinase. Since both Cdc5p and Sit4p have established roles in cell cycle regulation<span><span>, we investigated whether Atp2-T124/T317 phosphorylation was cell cycle-related. We present evidence that Atp2p levels and phosphorylation vary during cell cycle progression, with an increase at G2/M phase. Atp2-T124/T317 phosphorylation stimulates </span>mitochondrial membrane potential<span>, respiration and ATP levels at G2/M phase, indicating that dynamic Atp2p phosphorylation contributes to mitochondrial activity at this specific cell cycle phase. Preventing Atp2p phosphorylation delays G2/M to G1 transition, suggesting that enhanced </span></span></span>bioenergetics<span> at G2/M may help meet the energetic demands of cell cycle progression. However, mimicking constitutive T124/T317 phosphorylation or overexpressing Atp2p leads to mitochondrial DNA instability, indicating that reversible Atp2p phosphorylation is critical for homeostasis.</span></p><p>These results indicate that transient phosphorylation of Atp2p, a protein at the core of the ATP production machinery, impacts on mitochondrial bioenergetics and supports cell cycle progression at G2/M.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"85 ","pages":"Article 100905"},"PeriodicalIF":0.0,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10739574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphorylation-mediated regulation of the Nem1-Spo7/Pah1 phosphatase cascade in yeast lipid synthesis","authors":"Shoily Khondker,&nbsp;Gil-Soo Han,&nbsp;George M. Carman","doi":"10.1016/j.jbior.2022.100889","DOIUrl":"10.1016/j.jbior.2022.100889","url":null,"abstract":"<div><p>The <em>PAH1</em>-encoded phosphatidate phosphatase, which catalyzes the dephosphorylation of phosphatidate to produce diacylglycerol, controls the divergence of phosphatidate into triacylglycerol synthesis and phospholipid synthesis. Pah1 is inactive in the cytosol as a phosphorylated form and becomes active on the nuclear/endoplasmic reticulum membrane as a dephosphorylated form by the Nem1-Spo7 protein phosphatase complex. The phosphorylation of Pah1 by protein kinases, which include casein kinases I and II, Pho85-Pho80, Cdc28-cyclin B, and protein kinases A and C, controls its cellular location, catalytic activity, and susceptibility to proteasomal degradation. Nem1 (catalytic subunit) and Spo7 (regulatory subunit), which form a protein phosphatase complex catalyzing the dephosphorylation of Pah1 for its activation, are phosphorylated by protein kinases A and C. In this review, we discuss the functions and interrelationships of the protein kinases in the control of the Nem1-Spo7/Pah1 phosphatase cascade and lipid synthesis.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"84 ","pages":"Article 100889"},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9378635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CARD11 signaling in regulatory T cell development and function","authors":"Nicole M. Carter,&nbsp;Joel L. Pomerantz","doi":"10.1016/j.jbior.2022.100890","DOIUrl":"10.1016/j.jbior.2022.100890","url":null,"abstract":"<div><p>Regulatory T cells (Tregs) are a critical subset of CD4 T cells that modulate the immune response to prevent autoimmunity and chronic inflammation. CARD11, a signaling hub and scaffold protein that links antigen receptor engagement to activation of NF-κB and other downstream signaling pathways, is essential for the development and function of thymic Tregs. Mouse models with deficiencies in CARD11 and CARD11-associated signaling components generally have Treg defects, but some mouse models develop overt autoimmunity and inflammatory disease whereas others do not. Inhibition of CARD11 signaling in Tregs within the tumor microenvironment can potentially promote anti-tumor immunity. In this review, we summarize evidence for the involvement of CARD11 signaling in Treg development and function and discuss key unanswered questions and future research opportunities.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"84 ","pages":"Article 100890"},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9732571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum regarding missing Declaration of Competing Interest statements in previously published articles","authors":"","doi":"10.1016/j.jbior.2021.100855","DOIUrl":"10.1016/j.jbior.2021.100855","url":null,"abstract":"","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"84 ","pages":"Article 100855"},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2212492621000737/pdfft?md5=81a0066005a9ae1b455c08897295c00a&pid=1-s2.0-S2212492621000737-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39612451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum regarding missing Declaration of Competing Interest statements in previously published articles","authors":"","doi":"10.1016/j.jbior.2021.100856","DOIUrl":"10.1016/j.jbior.2021.100856","url":null,"abstract":"","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"84 ","pages":"Article 100856"},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2212492621000749/pdfft?md5=f2a11c05ca7ecea869fa934008817163&pid=1-s2.0-S2212492621000749-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39612453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New strategies for combating fungal infections: Inhibiting inositol lipid signaling by targeting Sec14 phosphatidylinositol transfer proteins","authors":"Vytas A. Bankaitis ,&nbsp;Ashutosh Tripathi ,&nbsp;Xiao-Ru Chen ,&nbsp;Tatyana I. Igumenova","doi":"10.1016/j.jbior.2022.100891","DOIUrl":"10.1016/j.jbior.2022.100891","url":null,"abstract":"<div><p>Virulent fungi represent a particularly difficult problem in the infectious disease arena as these organisms are eukaryotes that share many orthologous activities with their human hosts. The fact that these activities are often catalyzed by conserved proteins places additional demands on development of pharmacological strategies for specifically inhibiting target fungal activities without imposing undesirable secondary effects on the host. While deployment of a limited set of anti-mycotics has to date satisfied the clinical needs for treatment of fungal infections, the recent emergence of multi-drug resistant fungal ‘superbugs’ now poses a serious global health threat with rapidly diminishing options for treatment. This escalating infectious disease problem emphasizes the urgent need for development of new classes of anti-mycotics. In that regard, Sec14 phosphatidylinositol transfer proteins offer interesting possibilities for interfering with fungal phosphoinositide signaling with exquisite specificity and without targeting the highly conserved lipid kinases responsible for phosphoinositide production. Herein, we review the establishment of proof-of-principle that demonstrates the feasibility of such an approach. We also describe the lead compounds of four chemotypes that directly target fungal Sec14 proteins. The rules that pertain to the mechanism(s) of Sec14 inhibition by validated small molecule inhibitors, and the open questions that remain, are discussed – as are the challenges that face development of next generation Sec14-directed inhibitors.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"84 ","pages":"Article 100891"},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9379472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CCAAT enhancer binding protein gamma (C/EBP-γ): An understudied transcription factor","authors":"Zachary Renfro ,&nbsp;Bryan E. White ,&nbsp;Kimberly E. Stephens","doi":"10.1016/j.jbior.2022.100861","DOIUrl":"10.1016/j.jbior.2022.100861","url":null,"abstract":"<div><p><span>The CCAAT enhancer binding protein (C/EBP) family of transcription factors are important transcriptional mediators of a wide range of physiologic processes. C/EBP-</span><em>γ</em> is the shortest C/EBP protein and lacks a canonical activation domain for the recruitment of transcriptional machinery. Despite its ubiquitous expression and ability to dimerize with other C/EBP proteins, C/EBP-<em>γ</em> has been studied far less than other C/EBP proteins, and, to our knowledge, no review of its functions has been written. This review seeks to integrate the current knowledge about C/EBP-<em>γ</em><span> and its physiologic roles, especially in cell proliferation<span>, the integrated stress response, oncogenesis, hematopoietic and nervous system development, and metabolism, as well as to identify areas for future research.</span></span></p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"84 ","pages":"Article 100861"},"PeriodicalIF":0.0,"publicationDate":"2022-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9747211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochemical basis for an interaction between SNX27 and the flexible SNX1 N-terminus","authors":"Mintu Chandra ,&nbsp;Brett M. Collins ,&nbsp;Lauren P. Jackson","doi":"10.1016/j.jbior.2021.100842","DOIUrl":"10.1016/j.jbior.2021.100842","url":null,"abstract":"<div><p><span><span>Metazoans require the sorting nexin (SNX) protein, </span>SNX27<span><span>, to recycle hundreds of important transmembrane protein receptors from endosomes to the plasma membrane. Cargo recycling by SNX27 requires its interaction with </span>retromer<span>, a heterotrimer known to assemble on membranes with multiple sorting nexins, including SNX-BAR proteins and SNX3<span>. SNX27 has also been functionally linked to SNX-BARs, but the molecular basis of this interaction has been unknown. We identify a direct biochemical interaction between the conserved and flexible SNX1/SNX2 N-terminus and full-length SNX27 using purified proteins in pulldown experiments. Sequence alignments<span> indicate both SNX1 and SNX2 contain two short and conserved stretches of acidic residues bearing a DxF motif in their flexible N-terminal regions. Biochemical pulldown and mapping experiments reveal forty residues in the N-terminus of either SNX1 or SNX2 can mediate binding to SNX27. SNX27 truncation analysis demonstrates the SNX27 FERM domain<span> binds the SNX1 N-terminus. Calorimetry experiments quantified binding between the SNX1 N-terminus and SNX27 in the low micromolar affinity range (K</span></span></span></span></span></span>_D ∼10 μM) and suggest the second DxF motif may play a more prominent role in binding. Mutation of either DxF sequence in SNX1 abrogates measurable binding to SNX27 in the calorimeter. Modelling from both predicted and experimentally determined structures suggests the SNX27 FERM domain could accommodate both DxF motifs simultaneously. Together, these data suggest SNX27 is directly linked to specific SNX-BAR proteins through binding acidic motifs in the SNX1 or SNX2 N-terminus.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"83 ","pages":"Article 100842"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10456835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The inositol pyrophosphate metabolism of Dictyostelium discoideum does not regulate inorganic polyphosphate (polyP) synthesis","authors":"Yann Desfougères ,&nbsp;Paloma Portela-Torres ,&nbsp;Danye Qiu ,&nbsp;Thomas M. Livermore ,&nbsp;Robert K. Harmel ,&nbsp;Filipy Borghi ,&nbsp;Henning J. Jessen ,&nbsp;Dorothea Fiedler ,&nbsp;Adolfo Saiardi","doi":"10.1016/j.jbior.2021.100835","DOIUrl":"10.1016/j.jbior.2021.100835","url":null,"abstract":"<div><p>Initial studies on the inositol phosphates metabolism were enabled by the social amoeba <em>Dictyostelium discoideum.</em> The abundant amount of inositol hexakisphosphate (IP₆ also known as Phytic acid) present in the amoeba allowed the discovery of the more polar inositol pyrophosphates, IP₇ and IP₈, possessing one or two high energy phosphoanhydride bonds, respectively. Considering the contemporary growing interest in inositol pyrophosphates, it is surprising that in recent years <em>D. discoideum</em>, has contributed little to our understanding of their metabolism and function. This work fulfils this lacuna, by analysing the <em>ip6k, ppip5k</em> and <em>ip6k-ppip5K</em> amoeba null strains using PAGE, ¹³C-NMR and CE-MS analysis. Our study reveals an inositol pyrophosphate metabolism more complex than previously thought. The amoeba Ip6k synthesizes the 4/6-IP₇ in contrast to the 5-IP₇ isomer synthesized by the mammalian homologue. The amoeba Ppip5k synthesizes the same 1/3-IP₇ as the mammalian enzyme. In <em>D. discoideum</em>, the <em>ip6k</em> strain possesses residual amounts of IP₇. The residual IP₇ is also present in the <em>ip6k-ppip5K</em> strain, while the <em>ppip5k</em> single mutant shows a decrease in both IP₇ and IP₈ levels. This phenotype is in contrast to the increase in IP₇ observable in the yeast <em>vip1</em>Δ strain. The presence of IP₈ in <em>ppip5k</em> and the presence of IP₇ in <em>ip6k-ppip5K</em> indicate the existence of an additional inositol pyrophosphate synthesizing enzyme. Additionally, we investigated the existence of a metabolic relationship between inositol pyrophosphate synthesis and inorganic polyphosphate (polyP) metabolism as observed in yeast. These studies reveal that contrary to the yeast, Ip6k and Ppip5k do not control polyP cellular level in amoeba.</p></div>","PeriodicalId":7214,"journal":{"name":"Advances in biological regulation","volume":"83 ","pages":"Article 100835"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8885430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39627613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}