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Artikel ; Online: Global developmental delay and a de novo deletion of the 16p13.13 region.

Krakowski, Aneta / Hoang, Ny / Trost, Brett / Summers, Jane / Ambrozewicz, Patricia / Vorstman, Jacob

BMJ case reports

2024 Band 17, Heft 2

Abstract: Many rare genetic variants are associated with the risk of atypical neurodevelopmental trajectories. In this study, we report a patient with developmental delay, autistic traits and multiple congenital anomalies, including congenital heart anomalies and ... ...

Abstract	Many rare genetic variants are associated with the risk of atypical neurodevelopmental trajectories. In this study, we report a patient with developmental delay, autistic traits and multiple congenital anomalies, including congenital heart anomalies and orofacial cleft, with a 0.832 Mb de novo deletion of the 16p13.13 region classified as a variant of uncertain significance. Comparison of similar sized deletions and duplications overlapping the same genes in the DECIPHER database, revealed seven reports of copy number variants (CNVs), four duplications and three deletions. A neurodevelopmental phenotype including learning disability and intellectual disability was noted in some of the DECIPHER entries where phenotype was provided. Although the association between a deletion in this region and an atypical neurodevelopmental trajectory remains to be elucidated, the overlapping CNVs with neurodevelopmental phenotypes suggests possible candidate genes within the 16p13.13 region.
Mesh-Begriff(e)	Humans ; Cleft Lip ; Cleft Palate ; Intellectual Disability/genetics ; Abnormalities, Multiple/genetics ; DNA Copy Number Variations/genetics
Sprache	Englisch
Erscheinungsdatum	2024-02-28
Erscheinungsland	England
Dokumenttyp	Case Reports ; Journal Article
ISSN	1757-790X
ISSN (online)	1757-790X
DOI	10.1136/bcr-2022-251521
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Complex Autism Spectrum Disorder in a Patient with a Novel De Novo Heterozygous

Yip, Silas / Calli, Kristina / Qiao, Ying / Trost, Brett / Scherer, Stephen W / Lewis, M E Suzanne

Genes

2023 Band 14, Heft 12

Abstract: Autism spectrum disorder (ASD) comprises a group of complex neurodevelopmental features seen in many different forms due to variable causes. Highly impactful ASD-susceptibility genes are involved in pathways associated with brain development, chromatin ... ...

Abstract	Autism spectrum disorder (ASD) comprises a group of complex neurodevelopmental features seen in many different forms due to variable causes. Highly impactful ASD-susceptibility genes are involved in pathways associated with brain development, chromatin remodeling, and transcription regulation. In this study, we investigate a proband with complex ASD. Whole genome sequencing revealed a novel de novo missense mutation of a highly conserved amino acid residue (NP_001289981.1:p.His516Gln; chr2:1917275; hg38) in the
Mesh-Begriff(e)	Humans ; Autism Spectrum Disorder/genetics ; Phenotype ; Mutation, Missense ; Genetic Association Studies ; Gene Expression Regulation ; Nerve Tissue Proteins/genetics ; Transcription Factors/genetics
Chemische Substanzen	MYT1L protein, human ; Nerve Tissue Proteins ; Transcription Factors
Sprache	Englisch
Erscheinungsdatum	2023-11-24
Erscheinungsland	Switzerland
Dokumenttyp	Case Reports
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes14122122
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Discovery of genomic variation across a generation.

Trost, Brett / Loureiro, Livia O / Scherer, Stephen W

Human molecular genetics

2020 Band 30, Heft R2, Seite(n) R174–R186

Abstract: Over the past 30 years (the timespan of a generation), advances in genomics technologies have revealed tremendous and unexpected variation in the human genome and have provided increasingly accurate answers to long-standing questions of how much genetic ... ...

Abstract	Over the past 30 years (the timespan of a generation), advances in genomics technologies have revealed tremendous and unexpected variation in the human genome and have provided increasingly accurate answers to long-standing questions of how much genetic variation exists in human populations and to what degree the DNA complement changes between parents and offspring. Tracking the characteristics of these inherited and spontaneous (or de novo) variations has been the basis of the study of human genetic disease. From genome-wide microarray and next-generation sequencing scans, we now know that each human genome contains over 3 million single nucleotide variants when compared with the ~ 3 billion base pairs in the human reference genome, along with roughly an order of magnitude more DNA-approximately 30 megabase pairs (Mb)-being 'structurally variable', mostly in the form of indels and copy number changes. Additional large-scale variations include balanced inversions (average of 18 Mb) and complex, difficult-to-resolve alterations. Collectively, ~1% of an individual's genome will differ from the human reference sequence. When comparing across a generation, fewer than 100 new genetic variants are typically detected in the euchromatic portion of a child's genome. Driven by increasingly higher-resolution and higher-throughput sequencing technologies, newer and more accurate databases of genetic variation (for instance, more comprehensive structural variation data and phasing of combinations of variants along chromosomes) of worldwide populations will emerge to underpin the next era of discovery in human molecular genetics.
Mesh-Begriff(e)	Female ; Genetic Variation ; Genome, Human ; Genome-Wide Association Study ; Genomics/methods ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Mutation ; Whole Genome Sequencing
Sprache	Englisch
Erscheinungsdatum	2020-05-12
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddab209
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Conservation of kinase-phosphorylation site pairings: Evidence for an evolutionarily dynamic phosphoproteome.

McDonald, Megan / Trost, Brett / Napper, Scott

PloS one

2018 Band 13, Heft 8, Seite(n) e0202036

Abstract: Kinase-mediated protein phosphorylation is a central mechanism for regulation of cellular responses and phenotypes. While considerable information is available regarding the evolutionary relationships within the kinase family, as well as the evolutionary ...

Abstract	Kinase-mediated protein phosphorylation is a central mechanism for regulation of cellular responses and phenotypes. While considerable information is available regarding the evolutionary relationships within the kinase family, as well as the evolutionary conservation of phosphorylation sites, each aspect of this partnership is typically considered in isolation, despite their clear functional relationship. Here, to offer a more holistic perspective on the evolution of protein phosphorylation, the conservation of protein phosphorylation sites is considered in the context of the conservation of the corresponding modifying kinases. Specifically, conservation of defined kinase-phosphorylation site pairings (KPSPs), as well as of each of the component parts (the kinase and the phosphorylation site), were examined across a range of species. As expected, greater evolutionary distance between species was generally associated with lower probability of KPSP conservation, and only a small fraction of KPSPs were maintained across all species, with the vast majority of KPSP losses due to the absence of the phosphorylation site. This supports a model in which a relatively stable kinome promotes the emergence of functional substrates from an evolutionarily malleable phosphoproteome.
Mesh-Begriff(e)	Animals ; Biological Evolution ; Humans ; Models, Biological ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases/metabolism ; Proteome ; Proteomics/methods
Chemische Substanzen	Phosphoproteins ; Proteome ; Phosphotransferases (EC 2.7.-)
Sprache	Englisch
Erscheinungsdatum	2018-08-14
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0202036
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Complex Autism Spectrum Disorder with Epilepsy, Strabismus and Self-Injurious Behaviors in a Patient with a De Novo Heterozygous

Evans, Daniel R / Qiao, Ying / Trost, Brett / Calli, Kristina / Martell, Sally / Jones, Steven J M / Scherer, Stephen W / Lewis, M E Suzanne

Genes

2022 Band 13, Heft 3

Abstract: Autism spectrum disorder (ASD) describes a complex and heterogenous group of neurodevelopmental disorders. Whole genome sequencing continues to shed light on the multifactorial etiology of ASD. Dysregulated transcriptional pathways have been implicated ... ...

Abstract	Autism spectrum disorder (ASD) describes a complex and heterogenous group of neurodevelopmental disorders. Whole genome sequencing continues to shed light on the multifactorial etiology of ASD. Dysregulated transcriptional pathways have been implicated in neurodevelopmental disorders. Emerging evidence suggests that de novo POLR2A variants cause a newly described phenotype called ‘Neurodevelopmental Disorder with Hypotonia and Variable Intellectual and Behavioral Abnormalities’ (NEDHIB). The variable phenotype manifests with a spectrum of features; primarily early onset hypotonia and delay in developmental milestones. In this study, we investigate a patient with complex ASD involving epilepsy and strabismus. Whole genome sequencing of the proband−parent trio uncovered a novel de novo POLR2A variant (c.1367T>C, p. Val456Ala) in the proband. The variant appears deleterious according to in silico tools. We describe the phenotype in our patient, who is now 31 years old, draw connections between the previously reported phenotypes and further delineate this emerging neurodevelopmental phenotype. This study sheds new insights into this neurodevelopmental disorder, and more broadly, the genetic etiology of ASD.
Mesh-Begriff(e)	Autism Spectrum Disorder/genetics ; DNA-Directed RNA Polymerases/genetics ; Epilepsy/genetics ; Humans ; Intellectual Disability/genetics ; Muscle Hypotonia/genetics ; Self-Injurious Behavior ; Strabismus/genetics
Chemische Substanzen	DNA-Directed RNA Polymerases (EC 2.7.7.6) ; POLR2A RNA polymerase, human (EC 2.7.7.6)
Sprache	Englisch
Erscheinungsdatum	2022-03-07
Erscheinungsland	Switzerland
Dokumenttyp	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13030470
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Temporal analysis of enhancers during mouse cerebellar development reveals dynamic and novel regulatory functions.

Ramirez, Miguel / Badayeva, Yuliya / Yeung, Joanna / Wu, Joshua / Abdalla-Wyse, Ayasha / Yang, Erin / Trost, Brett / Scherer, Stephen W / Goldowitz, Daniel

eLife

2022 Band 11

Abstract: We have identified active enhancers in the mouse cerebellum at embryonic and postnatal stages which provides a view of novel enhancers active during cerebellar development. The majority of cerebellar enhancers have dynamic activity between embryonic and ... ...

Abstract	We have identified active enhancers in the mouse cerebellum at embryonic and postnatal stages which provides a view of novel enhancers active during cerebellar development. The majority of cerebellar enhancers have dynamic activity between embryonic and postnatal development. Cerebellar enhancers were enriched for neural transcription factor binding sites with temporally specific expression. Putative gene targets displayed spatially restricted expression patterns, indicating cell-type specific expression regulation. Functional analysis of target genes indicated that enhancers regulate processes spanning several developmental epochs such as specification, differentiation and maturation. We use these analyses to discover one novel regulator and one novel marker of cerebellar development: Bhlhe22 and Pax3, respectively. We identified an enrichment of de novo mutations and variants associated with autism spectrum disorder in cerebellar enhancers. Furthermore, by comparing our data with relevant brain development ENCODE histone profiles and cerebellar single-cell datasets we have been able to generalize and expand on the presented analyses, respectively. We have made the results of our analyses available online in the Developing Mouse Cerebellum Enhancer Atlas, where our dataset can be efficiently queried, curated and exported by the scientific community to facilitate future research efforts. Our study provides a valuable resource for studying the dynamics of gene expression regulation by enhancers in the developing cerebellum and delivers a rich dataset of novel gene-enhancer associations providing a basis for future in-depth studies in the cerebellum.
Mesh-Begriff(e)	Animals ; Autism Spectrum Disorder/genetics ; Enhancer Elements, Genetic ; Gene Expression Regulation, Developmental ; Mice ; Neurogenesis/genetics ; Transcription Factors/metabolism
Chemische Substanzen	Transcription Factors
Sprache	Englisch
Erscheinungsdatum	2022-08-09
Erscheinungsland	England
Dokumenttyp	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.74207
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Complex Autism Spectrum Disorder with Epilepsy, Strabismus and Self-Injurious Behaviors in a Patient with a De Novo Heterozygous POLR2A Variant

Evans, Daniel R. / Qiao, Ying / Trost, Brett / Calli, Kristina / Martell, Sally / Jones, Steven J. M. / Scherer, Stephen W. / Lewis, M. E. Suzanne

Genes. 2022 Mar. 07, v. 13, no. 3

2022

Abstract	Autism spectrum disorder (ASD) describes a complex and heterogenous group of neurodevelopmental disorders. Whole genome sequencing continues to shed light on the multifactorial etiology of ASD. Dysregulated transcriptional pathways have been implicated in neurodevelopmental disorders. Emerging evidence suggests that de novo POLR2A variants cause a newly described phenotype called ‘Neurodevelopmental Disorder with Hypotonia and Variable Intellectual and Behavioral Abnormalities’ (NEDHIB). The variable phenotype manifests with a spectrum of features; primarily early onset hypotonia and delay in developmental milestones. In this study, we investigate a patient with complex ASD involving epilepsy and strabismus. Whole genome sequencing of the proband–parent trio uncovered a novel de novo POLR2A variant (c.1367T>C, p. Val456Ala) in the proband. The variant appears deleterious according to in silico tools. We describe the phenotype in our patient, who is now 31 years old, draw connections between the previously reported phenotypes and further delineate this emerging neurodevelopmental phenotype. This study sheds new insights into this neurodevelopmental disorder, and more broadly, the genetic etiology of ASD.
Schlagwörter	autism ; computer simulation ; epilepsy ; etiology ; heterozygosity ; patients ; phenotype ; transcription (genetics)
Sprache	Englisch
Erscheinungsverlauf	2022-0307
Erscheinungsort	Multidisciplinary Digital Publishing Institute
Dokumenttyp	Artikel
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13030470
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Technological advances for interrogating the human kinome.

Baharani, Akanksha / Trost, Brett / Kusalik, Anthony / Napper, Scott

Biochemical Society transactions

2017 Band 45, Heft 1, Seite(n) 65–77

Abstract: There is increasing appreciation among researchers and clinicians of the value of investigating biology and pathobiology at the level of cellular kinase (kinome) activity. Kinome analysis provides valuable opportunity to gain insights into complex ... ...

Abstract	There is increasing appreciation among researchers and clinicians of the value of investigating biology and pathobiology at the level of cellular kinase (kinome) activity. Kinome analysis provides valuable opportunity to gain insights into complex biology (including disease pathology), identify biomarkers of critical phenotypes (including disease prognosis and evaluation of therapeutic efficacy), and identify targets for therapeutic intervention through kinase inhibitors. The growing interest in kinome analysis has fueled efforts to develop and optimize technologies that enable characterization of phosphorylation-mediated signaling events in a cost-effective, high-throughput manner. In this review, we highlight recent advances to the central technologies currently available for kinome profiling and offer our perspectives on the key challenges remaining to be addressed.
Mesh-Begriff(e)	Animals ; Humans ; Phosphorylation ; Protein Array Analysis/methods ; Protein Kinases/metabolism ; Proteome/metabolism ; Proteomics/methods ; Reproducibility of Results ; Signal Transduction
Chemische Substanzen	Proteome ; Protein Kinases (EC 2.7.-)
Sprache	Englisch
Erscheinungsdatum	2017-02-08
Erscheinungsland	England
Dokumenttyp	Journal Article ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20160163
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The Phenotypic variability of 16p11.2 distal BP2-BP3 deletion in a transgenerational family and in neurodevelopmentally ascertained samples.

Woodbury-Smith, Marc / D'Abate, Lia / Stavropoulos, Dimitri J / Howe, Jennifer / Drmic, Irene / Hoang, Ny / Zarrei, Mehdi / Trost, Brett / Iaboni, Alana / Anagnostou, Evdokia / Scherer, Stephen W

Journal of medical genetics

2023 Band 60, Heft 12, Seite(n) 1153–1160

Abstract: Background: We present genomic and phenotypic findings of a transgenerational family consisting of three male offspring, each with a maternally inherited distal 220 kb deletion at locus 16p11.2 (BP2-BP3). Genomic analysis of all family members was ... ...

Abstract	Background: We present genomic and phenotypic findings of a transgenerational family consisting of three male offspring, each with a maternally inherited distal 220 kb deletion at locus 16p11.2 (BP2-BP3). Genomic analysis of all family members was prompted by a diagnosis of autism spectrum disorder (ASD) in the eldest child, who also presented with a low body mass index. Methods: All male offspring underwent extensive neuropsychiatric evaluation. Both parents were also assessed for social functioning and cognition. The family underwent whole-genome sequencing. Further data curation was undertaken from samples ascertained for neurodevelopmental disorders and congenital abnormalities. Results: On medical examination, both the second and third-born male offspring presented with obesity. The second-born male offspring met research diagnostic criteria for ASD at 8 years of age and presented with mild attention deficits. The third-born male offspring was only noted as having motor deficits and received a diagnosis of developmental coordination disorder. Other than the 16p11.2 distal deletion, no additional contributing variants of clinical significance were observed. The mother was clinically evaluated and noted as having a broader autism phenotype. Conclusion: In this family, the phenotypes observed are most likely caused by the 16p11.2 distal deletion. The lack of other overt pathogenic mutations identified by genomic sequencing reinforces the variable expressivity that should be heeded in a clinical setting. Importantly, distal 16p11.2 deletions can present with a highly variable phenotype even within a single family. Our additional data curation provides further evidence on the variable clinical presentation among those with pathogenetic 16p11.2 (BP2-BP3) mutations.
Mesh-Begriff(e)	Child ; Humans ; Male ; Chromosome Deletion ; Autism Spectrum Disorder/diagnosis ; Autism Spectrum Disorder/genetics ; Autistic Disorder/genetics ; Family ; Phenotype ; Biological Variation, Population ; Chromosomes, Human, Pair 16/genetics ; Intellectual Disability/diagnosis ; Intellectual Disability/genetics
Sprache	Englisch
Erscheinungsdatum	2023-11-27
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	220881-7
ISSN	1468-6244 ; 0022-2593
ISSN (online)	1468-6244
ISSN	0022-2593
DOI	10.1136/jmg-2022-108818
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: DAPPLE 2: a Tool for the Homology-Based Prediction of Post-Translational Modification Sites

Trost, Brett / Maleki Farhad / Kusalik Anthony / Napper Scott

Journal of Proteome Research. 2016 Aug. 05, v. 15, no. 8

2016

Abstract: The post-translational modification of proteins is critical for regulating their function. Although many post-translational modification sites have been experimentally determined, particularly in certain model organisms, experimental knowledge of these ... ...

Abstract	The post-translational modification of proteins is critical for regulating their function. Although many post-translational modification sites have been experimentally determined, particularly in certain model organisms, experimental knowledge of these sites is severely lacking for many species. Thus, it is important to be able to predict sites of post-translational modification in such species. Previously, we described DAPPLE, a tool that facilitates the homology-based prediction of one particular post-translational modification, phosphorylation, in an organism of interest using known phosphorylation sites from other organisms. Here, we describe DAPPLE 2, which expands and improves upon DAPPLE in three major ways. First, it predicts sites for many post-translational modifications (20 different types) using data from several sources (15 online databases). Second, it has the ability to make predictions approximately 2–7 times faster than DAPPLE depending on the database size and the organism of interest. Third, it simplifies and accelerates the process of selecting predicted sites of interest by categorizing them based on gene ontology terms, keywords, and signaling pathways. We show that DAPPLE 2 can successfully predict known human post-translational modification sites using, as input, known sites from species that are either closely (e.g., mouse) or distantly (e.g., yeast) related to humans. DAPPLE 2 can be accessed at http://saphire.usask.ca/saphire/dapple2.
Schlagwörter	gene ontology ; humans ; mice ; models ; phosphorylation ; post-translational modification ; prediction ; proteins ; proteome ; signal transduction ; yeasts
Sprache	Englisch
Erscheinungsverlauf	2016-0805
Umfang	p. 2760-2767.
Erscheinungsort	American Chemical Society
Dokumenttyp	Artikel
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021%2Facs.jproteome.6b00304
Datenquelle	NAL Katalog (AGRICOLA)

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