Evolution of hemoglobin loci and their regulatory elements DOI
Sjaak Philipsen, Ross C. Hardison

Blood Cells Molecules and Diseases, Journal Year: 2017, Volume and Issue: 70, P. 2 - 12

Published: Aug. 9, 2017

Language: Английский

ESPEN micronutrient guideline DOI Creative Commons
Mette M. Berger,

Alan Shenkin,

Anna Schweinlin

et al.

Clinical Nutrition, Journal Year: 2022, Volume and Issue: 41(6), P. 1357 - 1424

Published: Feb. 26, 2022

Language: Английский

Citations

388

Hemoglobin: Structure, Function and Allostery DOI
Mostafa H. Ahmed, Mohini S. Ghatge, Martin K. Safo

et al.

Sub-cellular biochemistry/Subcellular biochemistry, Journal Year: 2020, Volume and Issue: unknown, P. 345 - 382

Published: Jan. 1, 2020

Language: Английский

Citations

199

Improving Protein Expression, Stability, and Function with ProteinMPNN DOI Creative Commons
Kiera H. Sumida, Reyes Núñez‐Franco, Indrek Kalvet

et al.

Journal of the American Chemical Society, Journal Year: 2024, Volume and Issue: 146(3), P. 2054 - 2061

Published: Jan. 9, 2024

Natural proteins are highly optimized for function but often difficult to produce at a scale suitable biotechnological applications due poor expression in heterologous systems, limited solubility, and sensitivity temperature. Thus, general method that improves the physical properties of native while maintaining could have wide utility protein-based technologies. Here, we show deep neural network ProteinMPNN, together with evolutionary structural information, provides route increasing protein expression, stability, function. For both myoglobin tobacco etch virus (TEV) protease, generated designs improved elevated melting temperatures, TEV identified multiple catalytic activity as compared parent sequence previously reported variants. Our approach should be broadly useful improving biotechnologically important proteins.

Language: Английский

Citations

109

Iron homeostasis imbalance and ferroptosis in brain diseases DOI Creative Commons
Haining Long,

Wangshu Zhu,

Liming Wei

et al.

MedComm, Journal Year: 2023, Volume and Issue: 4(4)

Published: June 26, 2023

Brain iron homeostasis is maintained through the normal function of blood-brain barrier and regulation at systemic cellular levels, which fundamental to brain function. Excess can catalyze generation free radicals Fenton reactions due its dual redox state, thus causing oxidative stress. Numerous evidence has indicated diseases, especially stroke neurodegenerative are closely related mechanism imbalance in brain. For one thing, diseases promote accumulation. another, accumulation amplifies damage nervous system exacerbates patients' outcomes. In addition, triggers ferroptosis, a newly discovered iron-dependent type programmed cell death, neurodegeneration received wide attention recent years. this context, we outline metabolism focus on current stroke, Alzheimer's disease, Parkinson's disease. Meanwhile, also discuss ferroptosis simultaneously enumerate drugs for chelators inhibitors.

Language: Английский

Citations

47

ESPEN practical short micronutrient guideline DOI Creative Commons
Mette M. Berger,

Alan Shenkin,

Oğuzhan Sıtkı Dizdar

et al.

Clinical Nutrition, Journal Year: 2024, Volume and Issue: 43(3), P. 825 - 857

Published: Jan. 30, 2024

BackgroundTrace elements and vitamins, named together micronutrients (MNs), are essential for human metabolism. The importance of MNs in common pathologies is recognized by recent research, with deficiencies significantly impacting the outcome.ObjectiveThis short version guideline aims to provide practical recommendations clinical practice.MethodsAn extensive search literature was conducted databases Medline, PubMed, Cochrane, Google Scholar, CINAHL initial guideline. focused on physiological data, historical evidence (for papers published before PubMed release 1996), observational and/or randomized trials. For each MN, main functions, optimal analytical methods, impact inflammation, potential toxicity, provision during enteral or parenteral nutrition were addressed. SOP wording applied strength recommendations.ResultsThe limited number interventional trials prevented meta-analysis led a low level most recommendations. underwent consensus process, which resulted percentage agreement (%): strong required >90 % votes. Altogether proposes 3 general specific 26 MNs. Monitoring management strategies proposed.ConclusionThis MN should facilitate handling at-risk diseases, whilst offering advice monitoring nutritional support.

Language: Английский

Citations

24

The transcription factor BACH1 at the crossroads of cancer biology: From epithelial–mesenchymal transition to ferroptosis DOI Creative Commons
Kazuhiko Igarashi, Hironari Nishizawa, Yuriko Saiki

et al.

Journal of Biological Chemistry, Journal Year: 2021, Volume and Issue: 297(3), P. 101032 - 101032

Published: July 30, 2021

The progression of cancer involves not only the gradual evolution cells by mutations in DNA but also alterations gene expression induced those and input from surrounding microenvironment. Such contribute to cells' abilities reprogram metabolic pathways undergo epithelial-to-mesenchymal transition (EMT), which facilitate survival their metastasis other organs. Recently, BTB CNC homology 1 (BACH1), a heme-regulated transcription factor that represses genes involved iron heme metabolism normal cells, was shown shape metastatic potential cells. growing list BACH1 target reveals promotes regulating various sets beyond metabolism. mediate cell–cell adhesion oxidative phosphorylation activates required for glycolysis, cell motility, matrix protein degradation. Furthermore, FOXA1 encoding an activator epithelial SNAI2 repressor genes, forming feedforward loop EMT. By synthesizing these observations, we propose "two-faced model", accounts dynamic switching between stress resistance along with progression. We discuss here possibility BACH1-mediated promotion brings increased sensitivity iron-dependent death (ferroptosis) through crosstalk imposing programmed vulnerability upon future directions this field, including dynamics plasticity Cancer are suggested reflect evolutionary process genetic modify giving rise variations. ensuing struggle existence (1Darwin J. Origin Species Means Natural Selection. Project Guttenberg, 1860Google Scholar) within body selects improved and/or adapted forms terms so-called hallmarks (2Hanahan D. Weinberg R.A. Hallmarks cancer: next generation.Cell. 2011; 144: 646-674Abstract Full Text PDF PubMed Scopus (35863) Google proliferation, invasion, metastasis, as well resistance. Some eventually dominate competing fellow During existence, alter properties functions changes response microenvironment therapeutic interventions (3Makohon-Moore A. Iacobuzio-Donahue C.A. Pancreatic biology genetics perspective.Nat. Rev. Cancer. 2016; 16: 553-565Crossref (197) Scholar). modulability expression, epigenetic alterations, may be another foundation evolution, heterogeneity thus formed allows selection better-fitted among genetically similar Therefore, some sinister such underlie difficulties treating patients cancer, entirely attributable alone. Metastasis depends on multiple steps local intravasation, extravasation, reproliferation (4Valastyan S. Tumor metastasis: Molecular insights evolving paradigms.Cell. 147: 275-292Abstract (2260) Epithelial-to-mesenchymal (EMT) can explain many incurred during reduces capability increases mobility invasiveness (5Dongre New into mechanisms epithelial-mesenchymal implications cancer.Nat. Mol. Cell Biol. 2019; 20: 69-84Crossref (787) Transcription factors known regulate EMT include ZEB1, ZEB2, SNAI1 (SNAIL), (SLUG), TWIST1 have been promote progression, Scholar, 6Puisieux Brabletz T. Caramel Oncogenic roles EMT-inducing factors.Nat. 2014; 488-494Crossref (581) 7Nieto M.A. Huang R.Y. Jackson Thiery J.P. Emt: 2016.Cell. 166: 21-45Abstract 8Stemmler M.P. Eccles R.L. Non-redundant 21: 102-112Crossref (155) However, direct EMT-related factors, shared them or unique one them, largely remain elusive (8Stemmler play critical placed under derived hostile microenvironments low oxygen, nutrients, glucose, attack immune Changes signaling impose endogenous stress. despite is dependent altered choreographed factors. Hypoxia-responsive (HIF1A) induces neoangiogenesis (9Ivan M. Kaelin Jr., W.G. EGLN-HIF O(2)-sensing system: Multiple inputs feedbacks.Mol. Cell. 2017; 66: 772-779Abstract 10Semenza G.L. Pharmacologic targeting hypoxia-inducible factors.Annu. Pharmacol. Toxicol. 59: 379-403Crossref (71) reprogramming glucose combination glycolysis (aerobic glycolysis) 11Luengo Li Z. Gui D.Y. Sullivan L.B. Zagorulya Do B.T. Ferreira R. Naamati Ali Lewis Thomas C.J. Spranger Matheson N.J. Vander Heiden M.G. Increased demand NAD(+) relative ATP drives aerobic glycolysis.Mol. 2021; 81: 691-707.e6Abstract (0) Heat shock HSF1 maintains homeostasis (12Fujimoto Takii Takaki E. Katiyar Nakato Shirahige K. Nakai HSF1-PARP13-PARP1 complex facilitates repair mammary tumorigenesis.Nat. Commun. 8: 1638Crossref (9) Activator protein-1 (AP-1) JUN FOS, characterized presence basic leucine zipper (bZip) DNA-binding domain, downstream effector molecules mitogen-activated kinase extracellular signal-regulated cascades against inflammation (13Bejjani F. Evanno Zibara Piechaczyk Jariel-Encontre I. AP-1 transcriptional complex: Local switch remote command?.Biochim. Biophys. Acta 1872: 11-23Crossref (40) NF-E2-related 2 (NFE2L2), bZip supports tumor proliferation part activating (14Kitamura H. Motohashi NRF2 addiction cells.Cancer Sci. 2018; 109: 900-911Crossref (102) 15Yamamoto Kensler T.W. KEAP1-NRF2 A thiol-based sensor-effector apparatus maintaining redox homeostasis.Physiol. 98: 1169-1203Crossref (407) 16Taguchi Yamamoto system molecular treatment.Cancers (Basel). 2020; 13Crossref (5) focus review (BACH1) (17Oyake Itoh Hayashi N. Hoshino Nishizawa Igarashi Bach proteins belong novel family BTB-basic interact MafK NF-E2 site.Mol. 1996; 6083-6095Crossref (477) 18Kanezaki Toki Yokoyama Yomogida Sugiyama Ito recruited nucleus its alternative spliced isoform.J. Chem. 2001; 276: 7278-7284Abstract Scholar), regulates iron- heme-related (19Igarashi Watanabe-Matsui Wearing red signaling: heme-bach axis metabolism, immunology.Tohoku Exp. Med. 232: 229-253Crossref (68) 20Kobayashi Kato Hada Itoh-Nakadai Fujiwara Muto Inoguchi Y. Ichiyanagi Hojo W. Tomosugi Sasaki Harigae Iron-heme-Bach1 erythroblast adaptation deficiency.Haematologica. 102: 454-465Crossref (14) Investigations types human cancers established via (Fig. 1, B). first structure, function, regulation factor. then summarize recent findings function examine how EMT, angiogenesis, epigenetics, explained based putative genes. model" integrate diverse additionally consider features plasticity, ferroptosis (iron-dependent death) shaped BACH1. These make compelling case examining key global understanding biology. Among there 61 constituting fourth most abundant after zinc finger, homeodomain, helix–loop–helix families (21Lambert S.A. Jolma Campitelli L.F. Das P.K. Yin Albu Chen X. Taipale Hughes T.R. Weirauch M.T. factors.Cell. 172: 650-665Abstract (535) further classified subfamilies according structural features. BACH2 broad-complex, tramtrack, bric-a-brac (BTB) domains 2A). closely related cap'n'collar (CNC) subfamily, short, evolutionarily conserved segment preceding domain. This originally found Drosophila (22Mohler Vani Leung Epstein Segmentally restricted, cephalic embryogenesis.Mech. Dev. 1991; 34: 3-9Crossref (107) etymology subfamily name derived. It binding (23Bean T.L. Ney P.A. regions p45 beta-globin erythroid cells.Nucleic Acids Res. 1997; 25: 2509-2515Crossref BACH1, BACH2, NFE2 (NF-E2 p45), NFE2L1 (NRF1), NFE2L2 (NF-E2-related 2), response, NFE2L3 (NRF3) (24Motohashi O'Connor Katsuoka Engel J.D. Integration diversity regulatory network composed Maf factors.Gene. 2002; 294: 1-12Crossref (363) NFE2, NFE2L1, NFE2L2, each linked four clusters HOX encode important plan development. Because quadruplication reflects two consecutive genome duplications vertebrates deuterostomes (25Kuraku Meyer maintenance Hox teleost-specific duplication.Int. 2009; 53: 765-773Crossref adopted specific vertebrate. In contrast, clusters, suggesting presumptive ancestor had separated BACH type before chordates, possess single homolog (26Amoutzias G.D. Veron A.S. Weiner Robinson-Rechavi Bornberg-Bauer Oliver S.G. Robertson D.L. One billion years bZIP evolution: Conservation change dimerization site specificity.Mol. Evol. 2007; 24: 827-835Crossref form heterodimers small MAF oncoproteins (MAFF, MAFG, MAFK) bind element referred recognition (MARE) (27Kataoka Noda nuclear oncoprotein recognizes sequences both Fos Jun.Mol. 1994; 14: 700-712Crossref recently CNC–sMAF–binding (28Otsuki Suzuki Tsuchida Suda Morita Shimizu Unique cistrome defined CsMBE strictly Nrf2-sMaf heterodimer cytoprotection.Free Radic. 91: 45-57Crossref (38) 29Otsuki Cis-element architecture sites relation diseases.Arch. Pharm. 43: 275-285Crossref 2B). MARE embeds motif protein-1, motifs bound FOS (30Igarashi Kurosaki Roychoudhuri innate adaptive immunity.Nat. Immunol. 17: 437-450Crossref (46) domain mediates homophilic interaction, hence, long-range interaction cis elements (31Igarashi Suwabe Nishikawa Nakauchi Multivalent generated Bach1 possible biochemical basis locus control region complex.J. 1998; 273: 11783-11790Abstract 32Yoshida C. Tokumasu Hohmura K.I. Bungert Nagasawa Takeyasu Long range cis-DNA mediated architectural Bach1.Genes Cells. 1999; 4: 643-655Crossref finger BCL6 corepressors (33Ahmad K.F. Melnick Lax Bouchard Liu Kiang C.L. Mayer Takahashi Licht Privé G.G. Mechanism SMRT corepressor recruitment domain.Mol. 2003; 12: 1551-1564Abstract (190) ubiquitin E3 ligase adaptor (34Słabicki Yoon Koeppel Nitsch L. Roy Burman S.S. Di Genua Donovan K.A. Sperling Hunkeler Tsai J.M. Sharma Guirguis Zou Chudasama P. Gasser J.A. et al.Small-molecule-induced polymerization triggers degradation BCL6.Nature. 588: 164-168Crossref (23) 35Wang Song Ye CRL3s: BTB-CUL3-RING ligases.Adv. 1217: 211-223Crossref (7) directly binds NANOG (36Niu Wang Guo Wei Jia Gong Qin Zhi Lu Gu Zhang Han J.J. Lan Meng recruits histone H3 lysine 4 methyltransferase MLL/SET1 complexes enhancer-promoter activity pluripotency.Nucleic 49: 1972-1986Crossref repressors recruiting NCOR1, NCOR2, deacetylases deacetylase (HDAC1) 3 (37Muto Madisen Yanai Obinata Karasuyama Groudine Identification Bach2 B-cell-specific partner negatively immunoglobulin heavy chain 3' enhancer.EMBO 5734-5743Crossref (150) 38Dohi Ikura Hoshikawa Katoh Ota Nakanome Omura Ohta Yoshida inhibits stress-induced cellular senescence impeding p53 chromatin.Nat. Struct. 2008; 15: 1246-1254Crossref (65) 39Tanaka Shima Sax Tajima Brydun Yoshizawa Masai Nio Ochiai Epigenetic Blimp-1 (Prdm1) B 3.J. 291: 6316-6330Abstract (39) 40Jiang Xu Sun suppresses developmental angiogenesis zebrafish.Oxid. Longev. 2017: 2143875Crossref (16) embed site, compete repress 2B) Note while regulated necessarily recognized longer than antagonistic relationship T activation differentiation (41Roychoudhuri Hirahara Mousavi Clever Klebanoff Bonelli Sciumè G. Zare Vahedi Dema B. Yu Rao Muranski Crompton J.G. al.BACH2 programs stabilize T(reg)-mediated homeostasis.Nature. 2013; 498: 506-510Crossref (248) 42Roychoudhuri Wakabayashi Quinn K.M. Ji Sukumar Eil Spolski Palmer D.C. Pan J.H. Patel S.J. Macallan CD8(+) controlling access enhancers.Nat. 851-860Crossref 43Kuwahara Ise Ochi Kometani Maruyama Izumoto Matsumoto Takemori Shinoda Nakayama Ohara O. Yasukawa Sawasaki al.Bach2-Batf interactions Th2-type IL-4 amplification loop.Nat. 7: 12596Crossref (43) heme, prosthetic group transport oxygen electron (44Ogawa Taketani Nakajima Nishitani Sassa Shibahara Fujita Heme derepression Bach1.EMBO 2835-2843Crossref (384) 45Hira Tomita Matsui Ikeda-Saito Bach1, heme-dependent factor, distinct coordination structure.IUBMB Life. 542-551Crossref (75) 46Watanabe-Matsui Murayama B-cell differentiation, antibody class switch, oxygenase-1 ligand Bach2.Blood. 117: 5438-5448Crossref (63) 47Watanabe-Matsui intrinsically disordered alters conformation.Arch. Biochem. 2015; 565: 25-31Crossref (22) 48Suenaga Uejima Shirouzu Charge-state-distribution analysis region.J. 160: 291-298Crossref 49Segawa Functional C-terminal repressor.Tohoku 247: 153-159Crossref 50Segawa Tsuda Biophysical characterization Bach1.Eur. 48: 361-369Crossref together proteins, suggest new sensors gas (51Shimizu Lengalova Martínek V. Martínková Heme: Emergent signal transduction, functional catalytic centres.Chem. Soc. 5624-5657Crossref Conventional globin, myoglobin, cytochrome c, well-structured (52Gell D.A. Structure haemoglobins.Blood Cells Dis. 70: 13-42Crossref (50) cysteine–proline embedded 53Sun Brand Zenke Tashiro exchange network.Proc. Natl. Acad. U. 2004; 101: 1461-1466Crossref (270) export (54Suzuki Hira Yamazaki triggering Crm1-dependent 23: 2544-2553Crossref (153) 55Suzuki Doi Satomi Cadmium gene.J. 278: 49246-49253Abstract (128) polyubiquitination, subsequent (46Watanabe-Matsui 56Zenke-Kawasaki Dohi Asahara Tokunaga Iwai ubiquitination Bach1.Mol. 27: 6962-6971Crossref (185) 2C). utilization mobilization iron, HMOX1 (HO-1) (57Sun Takaku Alam Taketo M.M. Hemoprotein enhancer availability gene.EMBO 5216-5224Crossref (460) FTH1 FTL ferritin heavy- light-chain subunits (58Hintze K.J. Theil E.C. repression thioredoxin reductase1 heme-sensitive vitro coordinates oxygenase1, beta-globin, NADP(H) quinone (oxido) reductase1.J. 282: 34365-34371Abstract SLC40A1 ferroporti

Language: Английский

Citations

72

A Multiple-Hit Hypothesis Involving Reactive Oxygen Species and Myeloperoxidase Explains Clinical Deterioration and Fatality in COVID-19 DOI Creative Commons

Pravin T. Goud,

David Bai,

Husam M. Abu‐Soud

et al.

International Journal of Biological Sciences, Journal Year: 2020, Volume and Issue: 17(1), P. 62 - 72

Published: Nov. 6, 2020

Multi-system involvement and rapid clinical deterioration are hallmarks of coronavirus disease 2019 (COVID-19) related mortality. The unique phenomena in severe COVID-19 can be perplexing, they include disproportionately hypoxemia relative to lung alveolar-parenchymal pathology deterioration, with poor response O

Language: Английский

Citations

71

The Role of Acidosis in the Pathogenesis of Severe Forms of COVID-19 DOI Creative Commons

Yury D. Nechipurenko,

Denis Semyonov, I. A. Lavrinenko

et al.

Biology, Journal Year: 2021, Volume and Issue: 10(9), P. 852 - 852

Published: Aug. 31, 2021

COVID-19 has specific characteristics that distinguish this disease from many other infections. We suggest the pathogenesis of severe forms can be associated with acidosis. This review article discusses several mechanisms potentially linking damaging effects acidosis and shows existence a vicious cycle between development hypoxia in patients. At early stages disease, inflammation, difficulty gas exchange lungs thrombosis collectively contribute to onset In accordance Verigo-Bohr effect, decrease blood pH leads oxygen saturation, which contributes exacerbation results deterioration patient’s condition. A also cause conformational changes S-protein virus thus lead affinity avidity protective antibodies. Hypoxia dysregulation immune system multidirectional pro- anti-inflammatory reactions, resulting “cytokine storm”. review, we highlight potential importance supporting normal as an approach therapy.

Language: Английский

Citations

65

Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response DOI Open Access

Zhengnan Yuan,

Ladie Kimberly De La Cruz,

Xiaoxiao Yang

et al.

Pharmacological Reviews, Journal Year: 2022, Volume and Issue: 74(3), P. 825 - 875

Published: June 23, 2022

Carbon monoxide (CO) has been firmly established as an endogenous signaling molecule with a variety of pathophysiological and pharmacological functions, including immunomodulation, organ protection, circadian clock regulation, among many others. In terms its molecular mechanism(s) action, CO is known to bind large number hemoproteins at least 25 identified targets, hemoglobin, myoglobin, neuroglobin, cytochrome c oxidase, P450, soluble guanylyl cyclase, myeloperoxidase, some ion channels dissociation constant values spanning the range sub-nM high μM. Although CO's binding affinity targets extensively studied established, there pressing need incorporate such information into analysis biologic response in context dosage. Especially important understand reservoir role hemoglobin storage, transport, distribution, transfer. We critically review literature inject sense quantitative assessment our analyses various relationships affinity, concentration, target occupancy level, anticipated actions. hope that this presents picture overall landscape engagement stimulates additional research, helps move field direction examining individual all concentration available CO. believe work will help further understanding relationship functions eventual development CO-based therapeutics.

Significance Statement

The carbon therapeutic agent significantly rely on therapeutically relevant varying affinity. This examines by quantitatively analyzing intricate for CO, state carboxyhemoglobin provide holistic approach action

Language: Английский

Citations

42

Basic Mechanisms of Hemolysis-Associated Thrombo-Inflammation and Immune Dysregulation DOI
Jordan D. Dimitrov, Lubka T. Roumenina, Gina Perrella

et al.

Arteriosclerosis Thrombosis and Vascular Biology, Journal Year: 2023, Volume and Issue: 43(8), P. 1349 - 1361

Published: June 15, 2023

Independent of etiology, hemolytic diseases are associated with thrombosis, inflammation and immune dysregulation, all together contributing to organ damage poor outcome. Beyond anemia the loss anti-inflammatory functions red blood cells, hemolysis leads release damage-associated molecular patterns including ADP, hemoglobin, heme, which act through multiple receptors signaling pathways fostering a hyperinflammatory hypercoagulable state. Extracellular free heme is promiscuous alarmin capable triggering oxido-inflammatory thrombotic events by inducing activation platelets, endothelial innate cells as well coagulation complement cascades. In this review, we discuss main mechanisms and, in particular, drive thrombo-inflammatory milieu consequences on host response secondary infections.

Language: Английский

Citations

25