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Article ; Online: The widespread nature of Pack-TYPE transposons reveals their importance for plant genome evolution.

Gisby, Jack S / Catoni, Marco

2022 Volume 18, Issue 2, Page(s) e1010078

Abstract: Pack-TYPE transposable elements (TEs) are a group of non-autonomous DNA transposons found in plants. These elements can efficiently capture and shuffle coding DNA across the host genome, accelerating the evolution of genes. Despite their relevance for ... ...

Abstract	Pack-TYPE transposable elements (TEs) are a group of non-autonomous DNA transposons found in plants. These elements can efficiently capture and shuffle coding DNA across the host genome, accelerating the evolution of genes. Despite their relevance for plant genome plasticity, the detection and study of Pack-TYPE TEs are challenging due to the high similarity these elements have with genes. Here, we produced an automated annotation pipeline designed to study Pack-TYPE elements and used it to successfully annotate and analyse more than 10,000 new Pack-TYPE TEs in the rice and maize genomes. Our analysis indicates that Pack-TYPE TEs are an abundant and heterogeneous group of elements. We found that these elements are associated with all main superfamilies of Class II DNA transposons in plants and likely share a similar mechanism to capture new chromosomal DNA sequences. Furthermore, we report examples of the direct contribution of these TEs to coding genes, suggesting a generalised and extensive role of Pack-TYPE TEs in plant genome evolution.
MeSH term(s)	DNA Transposable Elements/genetics ; Evolution, Molecular ; Genome, Plant/genetics ; Oryza/genetics ; Zea mays/genetics
Chemical Substances	DNA Transposable Elements
Language	English
Publishing date	2022-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1010078
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Article ; Online: Longitudinal plasma proteomics reveals biomarkers of alveolar-capillary barrier disruption in critically ill COVID-19 patients.

Duijvelaar, Erik / Gisby, Jack / Peters, James E / Bogaard, Harm Jan / Aman, Jurjan

Nature communications

2024 Volume 15, Issue 1, Page(s) 744

Abstract: The pathobiology of respiratory failure in COVID-19 consists of a complex interplay between viral cytopathic effects and a dysregulated host immune response. In critically ill patients, imatinib treatment demonstrated potential for reducing invasive ... ...

Abstract	The pathobiology of respiratory failure in COVID-19 consists of a complex interplay between viral cytopathic effects and a dysregulated host immune response. In critically ill patients, imatinib treatment demonstrated potential for reducing invasive ventilation duration and mortality. Here, we perform longitudinal profiling of 6385 plasma proteins in 318 hospitalised patients to investigate the biological processes involved in critical COVID-19, and assess the effects of imatinib treatment. Nine proteins measured at hospital admission accurately predict critical illness development. Next to dysregulation of inflammation, critical illness is characterised by pathways involving cellular adhesion, extracellular matrix turnover and tissue remodelling. Imatinib treatment attenuates protein perturbations associated with inflammation and extracellular matrix turnover. These proteomic alterations are contextualised using external pulmonary RNA-sequencing data of deceased COVID-19 patients and imatinib-treated Syrian hamsters. Together, we show that alveolar capillary barrier disruption in critical COVID-19 is reflected in the plasma proteome, and is attenuated with imatinib treatment. This study comprises a secondary analysis of both clinical data and plasma samples derived from a clinical trial that was registered with the EU Clinical Trials Register (EudraCT 2020-001236-10, https://www.clinicaltrialsregister.eu/ctr-search/trial/2020-001236-10/NL ) and Netherlands Trial Register (NL8491, https://www.trialregister.nl/trial/8491 ).
MeSH term(s)	Humans ; COVID-19 ; Critical Illness ; SARS-CoV-2 ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/therapeutic use ; Proteomics ; Inflammation ; Biomarkers
Chemical Substances	Imatinib Mesylate (8A1O1M485B) ; Biomarkers
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-44986-w
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Article ; Online: ACBD3 Bioinformatic Analysis and Protein Expression in Breast Cancer Cells.

Houghton-Gisby, Jack / Kerslake, Rachel / Karteris, Emmanouil / Mokbel, Kefah / Harvey, Amanda J

International journal of molecular sciences

2022 Volume 23, Issue 16

Abstract: ... ...

Abstract	ACBD3
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Biomarkers, Tumor/genetics ; Breast Neoplasms/metabolism ; Computational Biology ; Female ; Humans ; Membrane Proteins/metabolism ; Neoplasm Recurrence, Local
Chemical Substances	ACBD3 protein, human ; Adaptor Proteins, Signal Transducing ; Biomarkers, Tumor ; Membrane Proteins
Language	English
Publishing date	2022-08-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23168881
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Article ; Online: Structural basis for recruitment of the CHK1 DNA damage kinase by the CLASPIN scaffold protein.

Day, Matthew / Parry-Morris, Sarah / Houghton-Gisby, Jack / Oliver, Antony W / Pearl, Laurence H

Structure (London, England : 1993)

2021 Volume 29, Issue 6, Page(s) 531–539.e3

Abstract: CHK1 is a protein kinase that functions downstream of activated ATR to phosphorylate multiple targets as part of intra-S and G2/M DNA damage checkpoints. Its role in allowing cells to survive replicative stress has made it an important target for anti- ... ...

Abstract	CHK1 is a protein kinase that functions downstream of activated ATR to phosphorylate multiple targets as part of intra-S and G2/M DNA damage checkpoints. Its role in allowing cells to survive replicative stress has made it an important target for anti-cancer drug discovery. Activation of CHK1 by ATR depends on their mutual interaction with CLASPIN, a natively unstructured protein that interacts with CHK1 through a cluster of phosphorylation sites in its C-terminal half. We have now determined the crystal structure of the kinase domain of CHK1 bound to a high-affinity motif from CLASPIN. Our data show that CLASPIN engages a conserved site on CHK1 adjacent to the substrate-binding cleft, involved in phosphate sensing in other kinases. The CLASPIN motif is not phosphorylated by CHK1, nor does it affect phosphorylation of a CDC25 substrate peptide, suggesting that it functions purely as a scaffold for CHK1 activation by ATR.
MeSH term(s)	Adaptor Proteins, Signal Transducing/chemistry ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Binding Sites ; Checkpoint Kinase 1/chemistry ; Checkpoint Kinase 1/genetics ; Checkpoint Kinase 1/metabolism ; Crystallography, X-Ray ; Humans ; Models, Molecular ; Mutation ; Phosphorylation ; Protein Binding ; Protein Conformation ; Protein Domains ; Sf9 Cells
Chemical Substances	Adaptor Proteins, Signal Transducing ; CLSPN protein, human ; CHEK1 protein, human (EC 2.7.11.1) ; Checkpoint Kinase 1 (EC 2.7.11.1)
Language	English
Publishing date	2021-03-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1213087-4
ISSN	1878-4186 ; 0969-2126
ISSN (online)	1878-4186
ISSN	0969-2126
DOI	10.1016/j.str.2021.03.007
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Article ; Online: Multi-omics identify falling LRRC15 as a COVID-19 severity marker and persistent pro-thrombotic signals in convalescence.

Gisby, Jack S / Buang, Norzawani B / Papadaki, Artemis / Clarke, Candice L / Malik, Talat H / Medjeral-Thomas, Nicholas / Pinheiro, Damiola / Mortimer, Paige M / Lewis, Shanice / Sandhu, Eleanor / McAdoo, Stephen P / Prendecki, Maria F / Willicombe, Michelle / Pickering, Matthew C / Botto, Marina / Thomas, David C / Peters, James E

Nature communications

2022 Volume 13, Issue 1, Page(s) 7775

Abstract: Patients with end-stage kidney disease (ESKD) are at high risk of severe COVID-19. Here, we perform longitudinal blood sampling of ESKD haemodialysis patients with COVID-19, collecting samples pre-infection, serially during infection, and after clinical ... ...

Abstract	Patients with end-stage kidney disease (ESKD) are at high risk of severe COVID-19. Here, we perform longitudinal blood sampling of ESKD haemodialysis patients with COVID-19, collecting samples pre-infection, serially during infection, and after clinical recovery. Using plasma proteomics, and RNA-sequencing and flow cytometry of immune cells, we identify transcriptomic and proteomic signatures of COVID-19 severity, and find distinct temporal molecular profiles in patients with severe disease. Supervised learning reveals that the plasma proteome is a superior indicator of clinical severity than the PBMC transcriptome. We show that a decreasing trajectory of plasma LRRC15, a proposed co-receptor for SARS-CoV-2, is associated with a more severe clinical course. We observe that two months after the acute infection, patients still display dysregulated gene expression related to vascular, platelet and coagulation pathways, including PF4 (platelet factor 4), which may explain the prolonged thrombotic risk following COVID-19.
MeSH term(s)	Humans ; COVID-19 ; Convalescence ; Multiomics ; SARS-CoV-2 ; Leukocytes, Mononuclear ; Proteomics ; Thrombosis ; Membrane Proteins
Chemical Substances	LRRC15 protein, human ; Membrane Proteins
Language	English
Publishing date	2022-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-35454-4
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Article ; Online: Plasma Lectin Pathway Complement Proteins in Patients With COVID-19 and Renal Disease.

Medjeral-Thomas, Nicholas R / Troldborg, Anne / Hansen, Annette G / Gisby, Jack / Clarke, Candice L / Prendecki, Maria / McAdoo, Stephen P / Sandhu, Eleanor / Lightstone, Liz / Thomas, David C / Willicombe, Michelle / Botto, Marina / Peters, James E / Pickering, Matthew C / Thiel, Steffen

Frontiers in immunology

2021 Volume 12, Page(s) 671052

Abstract: We do not understand why non-white ethnicity and chronic kidney disease increase susceptibility to COVID-19. The lectin pathway of complement activation is a key contributor to innate immunity and inflammation. Concentrations of plasma lectin pathway ... ...

Abstract	We do not understand why non-white ethnicity and chronic kidney disease increase susceptibility to COVID-19. The lectin pathway of complement activation is a key contributor to innate immunity and inflammation. Concentrations of plasma lectin pathway proteins influence pathway activity and vary with ethnicity. We measured circulating lectin proteins in a multi-ethnic cohort of chronic kidney disease patients with and without COVID19 infection to determine if lectin pathway activation was contributing to COVID19 severity. We measured 11 lectin proteins in serial samples from a cohort of 33 patients with chronic kidney impairment and COVID19. Controls were single plasma samples from 32 patients on dialysis and 32 healthy individuals. We demonstrated multiple associations between recognition molecules and associated proteases of the lectin pathway and COVID-19, including COVID-19 severity. Some of these associations were unique to patients of Asian and White ethnicity. Our novel findings demonstrate that COVID19 infection alters the concentration of plasma lectin proteins and some of these changes were linked to ethnicity. This suggests a role for the lectin pathway in the host response to COVID-19 and suggest that variability within this pathway may contribute to ethnicity-associated differences in susceptibility to severe COVID-19.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; COVID-19/blood ; COVID-19/ethnology ; COVID-19/immunology ; COVID-19/pathology ; Complement Pathway, Mannose-Binding Lectin ; Female ; Humans ; Lectins/blood ; Lectins/immunology ; Male ; Middle Aged ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/ethnology ; Renal Insufficiency, Chronic/immunology ; Renal Insufficiency, Chronic/pathology ; SARS-CoV-2/immunology ; SARS-CoV-2/metabolism
Chemical Substances	Lectins
Language	English
Publishing date	2021-04-29
Publishing country	Switzerland
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.671052
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Article ; Online: Multi-omics identify LRRC15 as a COVID-19 severity predictor and persistent pro-thrombotic signals in convalescence

medRxiv

Abstract: Patients with end-stage kidney disease (ESKD) are at high risk of severe COVID-19. Here, we performed longitudinal blood sampling of ESKD haemodialysis patients with COVID-19, collecting samples pre-infection, serially during infection, and after ... ...

Abstract	Patients with end-stage kidney disease (ESKD) are at high risk of severe COVID-19. Here, we performed longitudinal blood sampling of ESKD haemodialysis patients with COVID-19, collecting samples pre-infection, serially during infection, and after clinical recovery. Using plasma proteomics, and RNA-sequencing and flow cytometry of immune cells, we identified transcriptional and proteomic signatures of COVID-19 severity, and found distinct temporal molecular profiles in patients with severe disease. Supervised learning revealed that the plasma proteome is a superior indicator of clinical severity than the PBMC transcriptome. Notably, we show that both the levels and trajectory of plasma LRRC15, a proposed co-receptor for SARS-CoV-2, are the strongest predictors of clinical outcome. Strikingly, we observed that two months after the acute infection, patients still display dysregulated gene expression related to vascular, platelet and coagulation pathways, including PF4, providing a potential explanation for the prolonged elevation of thrombotic risk following COVID-19.
Keywords	covid19
Language	English
Publishing date	2022-05-01
Publisher	Cold Spring Harbor Laboratory Press
Document type	Article ; Online
DOI	10.1101/2022.04.29.22274267
Database	COVID19

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Article ; Online: Association of Histologic Parameters with Outcome in C3 Glomerulopathy and Idiopathic Immunoglobulin-Associated Membranoproliferative Glomerulonephritis.

Lomax-Browne, Hannah J / Medjeral-Thomas, Nicholas R / Barbour, Sean J / Gisby, Jack / Han, Heedeok / Bomback, Andrew S / Fervenza, Fernando C / Cairns, Thomas H / Szydlo, Richard / Tan, Sven-Jean / Marks, Stephen D / Waters, Aoife M / Appel, Gerald B / D'Agati, Vivette D / Sethi, Sanjeev / Nast, Cynthia C / Bajema, Ingeborg / Alpers, Charles E / Fogo, Agnes B /

Licht, Christoph / Fakhouri, Fadi / Cattran, Daniel C / Peters, James E / Cook, H Terence / Pickering, Matthew C

Clinical journal of the American Society of Nephrology : CJASN

2022 Volume 17, Issue 7, Page(s) 994–1007

Abstract: Background and objectives: C3 glomerulopathy and idiopathic Ig-associated membranoproliferative GN are kidney diseases characterized by abnormal glomerular complement C3 deposition. These conditions are heterogeneous in outcome, but approximately 50% of ...

Abstract	Background and objectives: C3 glomerulopathy and idiopathic Ig-associated membranoproliferative GN are kidney diseases characterized by abnormal glomerular complement C3 deposition. These conditions are heterogeneous in outcome, but approximately 50% of patients develop kidney failure within 10 years. Design, setting, participants, & measurements: To improve identification of patients with poor prognosis, we performed a detailed analysis of percutaneous kidney biopsies in a large cohort of patients. Using a validated histologic scoring system, we analyzed 156 native diagnostic kidney biopsies from a retrospective cohort of 123 patients with C3 glomerulopathy and 33 patients with Ig-associated membranoproliferative GN. We used linear regression, survival analysis, and Cox proportional hazards models to assess the relationship between histologic and clinical parameters with outcome. Results: Frequent biopsy features were mesangial expansion and hypercellularity, glomerular basement membrane double contours, and endocapillary hypercellularity. Multivariable analysis showed negative associations between eGFR and crescents, interstitial inflammation, and interstitial fibrosis/tubular atrophy. Proteinuria positively associated with endocapillary hypercellularity and glomerular basement membrane double contours. Analysis of second native biopsies did not demonstrate associations between immunosuppression treatment and improvement in histology. Using a composite outcome, risk of progression to kidney failure associated with eGFR and proteinuria at the time of biopsy, cellular/fibrocellular crescents, segmental sclerosis, and interstitial fibrosis/tubular atrophy scores. Conclusions: Our detailed assessment of kidney biopsy data indicated that cellular/fibrocellular crescents and interstitial fibrosis/tubular atrophy scores were significant determinants of deterioration in kidney function.
MeSH term(s)	Atrophy ; Biopsy ; Fibrosis ; Glomerulonephritis/diagnosis ; Glomerulonephritis, Membranoproliferative/pathology ; Humans ; Immunoglobulins ; Proteinuria/etiology ; Renal Insufficiency/complications ; Retrospective Studies
Chemical Substances	Immunoglobulins
Language	English
Publishing date	2022-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.16801221
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Article ; Online: Longitudinal proteomic profiling of dialysis patients with COVID-19 reveals markers of severity and predictors of death.

Gisby, Jack / Clarke, Candice L / Medjeral-Thomas, Nicholas / Malik, Talat H / Papadaki, Artemis / Mortimer, Paige M / Buang, Norzawani B / Lewis, Shanice / Pereira, Marie / Toulza, Frederic / Fagnano, Ester / Mawhin, Marie-Anne / Dutton, Emma E / Tapeng, Lunnathaya / Richard, Arianne C / Kirk, Paul Dw / Behmoaras, Jacques / Sandhu, Eleanor / McAdoo, Stephen P /

Prendecki, Maria F / Pickering, Matthew C / Botto, Marina / Willicombe, Michelle / Thomas, David C / Peters, James E

eLife

2021 Volume 10

Abstract: End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We measured 436 circulating proteins in serial blood samples from hospitalised and non-hospitalised ESKD patients with COVID-19 (n = 256 samples from 55 patients). Comparison ... ...

Abstract	End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We measured 436 circulating proteins in serial blood samples from hospitalised and non-hospitalised ESKD patients with COVID-19 (n = 256 samples from 55 patients). Comparison to 51 non-infected patients revealed 221 differentially expressed proteins, with consistent results in a separate subcohort of 46 COVID-19 patients. Two hundred and three proteins were associated with clinical severity, including IL6, markers of monocyte recruitment (e.g. CCL2, CCL7), neutrophil activation (e.g. proteinase-3), and epithelial injury (e.g. KRT19). Machine-learning identified predictors of severity including IL18BP, CTSD, GDF15, and KRT19. Survival analysis with joint models revealed 69 predictors of death. Longitudinal modelling with linear mixed models uncovered 32 proteins displaying different temporal profiles in severe versus non-severe disease, including integrins and adhesion molecules. These data implicate epithelial damage, innate immune activation, and leucocyte-endothelial interactions in the pathology of severe COVID-19 and provide a resource for identifying drug targets.
MeSH term(s)	Aged ; Biomarkers/blood ; COVID-19/blood ; COVID-19/mortality ; COVID-19/virology ; Female ; Forecasting ; Hospitalization ; Humans ; Kidney Failure, Chronic/blood ; Kidney Failure, Chronic/mortality ; Kidney Failure, Chronic/therapy ; Kidney Failure, Chronic/virology ; Longitudinal Studies ; Male ; Middle Aged ; Prognosis ; Proteomics/methods ; Renal Dialysis/methods ; Renal Dialysis/mortality ; SARS-CoV-2/isolation & purification ; Severity of Illness Index
Chemical Substances	Biomarkers
Language	English
Publishing date	2021-03-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.64827
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Article ; Online: Longitudinal proteomic profiling of dialysis patients with COVID-19 reveals markers of severity and predictors of death

Jack Gisby / Candice L Clarke / Nicholas Medjeral-Thomas / Talat H Malik / Artemis Papadaki / Paige M Mortimer / Norzawani B Buang / Shanice Lewis / Marie Pereira / Frederic Toulza / Ester Fagnano / Marie-Anne Mawhin / Emma E Dutton / Lunnathaya Tapeng / Arianne C Richard / Paul DW Kirk / Jacques Behmoaras / Eleanor Sandhu / Stephen P McAdoo /

Maria F Prendecki / Matthew C Pickering / Marina Botto / Michelle Willicombe / David C Thomas / James E Peters

eLife, Vol

2021 Volume 10

Abstract	End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We measured 436 circulating proteins in serial blood samples from hospitalised and non-hospitalised ESKD patients with COVID-19 (n = 256 samples from 55 patients). Comparison to 51 non-infected patients revealed 221 differentially expressed proteins, with consistent results in a separate subcohort of 46 COVID-19 patients. Two hundred and three proteins were associated with clinical severity, including IL6, markers of monocyte recruitment (e.g. CCL2, CCL7), neutrophil activation (e.g. proteinase-3), and epithelial injury (e.g. KRT19). Machine-learning identified predictors of severity including IL18BP, CTSD, GDF15, and KRT19. Survival analysis with joint models revealed 69 predictors of death. Longitudinal modelling with linear mixed models uncovered 32 proteins displaying different temporal profiles in severe versus non-severe disease, including integrins and adhesion molecules. These data implicate epithelial damage, innate immune activation, and leucocyte–endothelial interactions in the pathology of severe COVID-19 and provide a resource for identifying drug targets.
Keywords	COVID-19 ; proteomics ; longitudinal ; biomarkers ; cytokines ; end-stage kidney disease ; Medicine ; R ; Science ; Q ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	eLife Sciences Publications Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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