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Article ; Online: Phosphorylated nuclear DICER1 promotes open chromatin state and lineage plasticity of AT2 tumor cells in lung adenocarcinomas.

Reyes-Castro, Raisa A / Chen, Shin-Yu / Seemann, Jacob / Kundu, Samrat T / Gibbons, Don L / Arur, Swathi

2023 Volume 9, Issue 30, Page(s) eadf6210

Abstract: KRAS/ERK pathway phosphorylates DICER1, causing its nuclear translocation, and ... ...

Abstract	KRAS/ERK pathway phosphorylates DICER1, causing its nuclear translocation, and phosphomimetic
MeSH term(s)	Humans ; Mice ; Animals ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Chromatin/genetics ; MicroRNAs/genetics ; Adenocarcinoma of Lung/genetics ; Lung Neoplasms/genetics ; Ribonuclease III/genetics ; Ribonuclease III/metabolism ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism
Chemical Substances	Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Chromatin ; MicroRNAs ; DICER1 protein, human (EC 3.1.26.3) ; Ribonuclease III (EC 3.1.26.3) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2023-07-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adf6210
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Article ; Online: ZEB1 Is Regulated by K811 Acetylation to Promote Stability, NuRD Complex Interactions, EMT, and NSCLC Metastasis.

Perez-Oquendo, Mabel / Manshouri, Roxsan / Tian, Yanhua / Fradette, Jared J / Rodriguez, B Leticia / Kundu, Samrat T / Gibbons, Don L

Molecular cancer research : MCR

2023 Volume 21, Issue 8, Page(s) 779–794

Abstract: Epithelial-to-mesenchymal transition results in loss of specialized epithelial cell contacts and acquisition of mesenchymal invasive capacity. The transcription repressor zinc finger E-box-binding homeobox 1 (ZEB1) binds to E-boxes of gene promoter ... ...

Abstract	Epithelial-to-mesenchymal transition results in loss of specialized epithelial cell contacts and acquisition of mesenchymal invasive capacity. The transcription repressor zinc finger E-box-binding homeobox 1 (ZEB1) binds to E-boxes of gene promoter regions to suppress the expression of epithelial genes. ZEB1 has inconsistent molecular weights, which have been attributed to posttranslational modifications (PTM). We performed mass spectrometry and identified K811 acetylation as a novel PTM in ZEB1. To define the role of ZEB1 acetylation in regulating function, we generated ZEB1 acetyl-mimetic (K811Q) and acetyl-deficient (K811R) mutant-expressing non-small cell lung cancer cell lines (NSCLC). We demonstrate that the K811R ZEB1 (125 kDa) has a shorter protein half-life than wild-type (WT) ZEB1 and K811Q ZEB1 (∼225 kDa), suggesting that lack of ZEB1 acetylation in the lower molecular weight form affects protein stability. Further, the acetylated form of ZEB1 recruits the nucleosome remodeling and deacetylase (NuRD) complex to bind the promoter of its target genes mir200c-141 and SEMA3F. RNA-sequencing revealed that WT ZEB1 and K811Q ZEB1 downregulate the expression of epithelial genes to promote lung adenocarcinoma invasion and metastasis, whereas the K811R ZEB1 does not. Our findings establish that the K811 acetylation promotes ZEB1 protein stability, interaction with other protein complexes, and subsequent invasion/metastasis of lung adenocarcinoma via epithelial-to-mesenchymal transition. Implications: The molecular mechanisms by which ZEB1 is regulated by K811 acetylation to promote protein stability, NuRD complex and promoter interactions, and function are relevant to the development of treatment strategies to prevent and treat metastasis in patients with NSCLC.
MeSH term(s)	Humans ; Lung Neoplasms/pathology ; Carcinoma, Non-Small-Cell Lung/metabolism ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/genetics ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/metabolism ; Acetylation ; Zinc Finger E-box-Binding Homeobox 1/genetics ; Zinc Finger E-box-Binding Homeobox 1/metabolism ; Protein Processing, Post-Translational ; Adenocarcinoma of Lung/genetics ; Epithelial-Mesenchymal Transition/genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Membrane Proteins/genetics ; Nerve Tissue Proteins/genetics
Chemical Substances	Mi-2 Nucleosome Remodeling and Deacetylase Complex (EC 3.5.1.98) ; Zinc Finger E-box-Binding Homeobox 1 ; ZEB1 protein, human ; SEMA3F protein, human ; Membrane Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-22-0503
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Article ; Online: IMPAD1 and KDELR2 drive invasion and metastasis by enhancing Golgi-mediated secretion.

Bajaj, Rakhee / Kundu, Samrat T / Grzeskowiak, Caitlin L / Fradette, Jared J / Scott, Kenneth L / Creighton, Chad J / Gibbons, Don L

Oncogene

2020 Volume 39, Issue 37, Page(s) 5979–5994

Abstract: Non-small cell lung cancer (NSCLC) is the deadliest form of cancer worldwide, due in part to its proclivity to metastasize. Identifying novel drivers of invasion and metastasis holds therapeutic potential for the disease. We conducted a gain-of-function ... ...

Abstract	Non-small cell lung cancer (NSCLC) is the deadliest form of cancer worldwide, due in part to its proclivity to metastasize. Identifying novel drivers of invasion and metastasis holds therapeutic potential for the disease. We conducted a gain-of-function invasion screen, which identified two separate hits, IMPAD1 and KDELR2, as robust, independent drivers of lung cancer invasion and metastasis. Given that IMPAD1 and KDELR2 are known to be localized to the ER-Golgi pathway, we studied their common mechanism of driving in vitro invasion and in vivo metastasis and demonstrated that they enhance Golgi-mediated function and secretion. Therapeutically inhibiting matrix metalloproteases (MMPs) suppressed both IMPAD1- and KDELR2-mediated invasion. The hits from this unbiased screen and the mechanistic validation highlight Golgi function as one of the key cellular features altered during invasion and metastasis.
MeSH term(s)	Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Disease Progression ; Fluorescent Antibody Technique ; Gene Expression Regulation, Neoplastic ; Golgi Apparatus/metabolism ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Matrix Metalloproteinases/metabolism ; Neoplasm Invasiveness ; Phosphoric Monoester Hydrolases/genetics ; Phosphoric Monoester Hydrolases/metabolism ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism
Chemical Substances	Vesicular Transport Proteins ; KDELR2 protein, human (147097-18-5) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2020-08-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01410-z
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Zs.A 2218: Show issues

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Article ; Online: MBIP (MAP3K12 binding inhibitory protein) drives NSCLC metastasis by JNK-dependent activation of MMPs.

Ochieng, Joshua Kapere / Kundu, Samrat T / Bajaj, Rakhee / Leticia Rodriguez, B / Fradette, Jared J / Gibbons, Don L

Oncogene

2020 Volume 39, Issue 43, Page(s) 6719–6732

Abstract: Metastasis is the cause for 90% of cancer-related mortalities. Identification of genetic drivers promoting dissemination of tumor cells may provide opportunities for novel therapeutic strategies. We previously reported an in vivo gain-of-function screen ... ...

Abstract	Metastasis is the cause for 90% of cancer-related mortalities. Identification of genetic drivers promoting dissemination of tumor cells may provide opportunities for novel therapeutic strategies. We previously reported an in vivo gain-of-function screen that identified ~30 genes with a functional role in metastasis promotion and characterized detailed mechanistic functions of two hits. In this study, we characterized the contribution of one of the identified genes, MBIP (MAP3K12 binding inhibitory protein), towards driving tumor invasion and metastasis. We demonstrate that expression of MBIP significantly enhances the cellular proliferation, migration and invasion of NSCLC cells in vitro and metastasis in vivo. We functionally characterized that MBIP mediates activation of the JNK pathway and induces expression of matrix metalloproteinases (MMPs), which are necessary for the invasive and metastatic phenotype. Our findings establish a novel mechanistic role of MBIP as a driver of NSCLC progression and metastasis.
MeSH term(s)	Animals ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/secondary ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation/genetics ; Disease Models, Animal ; Disease Progression ; Female ; Gain of Function Mutation ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Male ; Matrix Metalloproteinases/metabolism ; Mice ; Neoplasm Invasiveness/genetics ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/pathology ; Xenograft Model Antitumor Assays
Chemical Substances	Intracellular Signaling Peptides and Proteins ; MBIP protein, human ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2020-09-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-020-01463-0
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Zs.A 2218: Show issues

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Article ; Online: Impad1 and Syt11 work in an epistatic pathway that regulates EMT-mediated vesicular trafficking to drive lung cancer invasion and metastasis.

Bajaj, Rakhee / Rodriguez, B Leticia / Russell, William K / Warner, Amanda N / Diao, Lixia / Wang, Jing / Raso, Maria G / Lu, Wei / Khan, Khaja / Solis, Luisa S / Batra, Harsh / Tang, Ximing / Fradette, Jared F / Kundu, Samrat T / Gibbons, Don L

Cell reports

2022 Volume 40, Issue 13, Page(s) 111429

Abstract: Lung cancer is a highly aggressive and metastatic disease responsible for approximately 25% of all cancer-related deaths in the United States. Using high-throughput in vitro and in vivo screens, we have previously established Impad1 as a driver of lung ... ...

Abstract	Lung cancer is a highly aggressive and metastatic disease responsible for approximately 25% of all cancer-related deaths in the United States. Using high-throughput in vitro and in vivo screens, we have previously established Impad1 as a driver of lung cancer invasion and metastasis. Here we elucidate that Impad1 is a direct target of the epithelial microRNAs (miRNAs) miR-200 and miR∼96 and is de-repressed during epithelial-to-mesenchymal transition (EMT); thus, we establish a mode of regulation of the protein. Impad1 modulates Golgi apparatus morphology and vesicular trafficking through its interaction with a trafficking protein, Syt11. These changes in Golgi apparatus dynamics alter the extracellular matrix and the tumor microenvironment (TME) to promote invasion and metastasis. Inhibiting Impad1 or Syt11 disrupts the cancer cell secretome, regulates the TME, and reverses the invasive or metastatic phenotype. This work identifies Impad1 as a regulator of EMT and secretome-mediated changes during lung cancer progression.
MeSH term(s)	Cell Line, Tumor ; Cell Movement ; Epithelial-Mesenchymal Transition/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/pathology ; MicroRNAs/metabolism ; Neoplasm Invasiveness/genetics ; Neoplasm Metastasis ; Synaptotagmins/metabolism ; Tumor Microenvironment
Chemical Substances	MicroRNAs ; SYT11 protein, human ; Synaptotagmins (134193-27-4)
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111429
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Article ; Online: Robust and specific inhibition of microRNAs in Caenorhabditis elegans.

Kundu, Samrat T / Slack, Frank J

Journal of biology

2010 Volume 9, Issue 3, Page(s) 20

Abstract: MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression of numerous target genes. Yet, while hundreds of miRNAs have been identified, little is known about their functions. In a recent report published in Silence, Zheng and colleagues ... ...

Abstract	MicroRNAs (miRNAs) are small non-coding RNAs that regulate the expression of numerous target genes. Yet, while hundreds of miRNAs have been identified, little is known about their functions. In a recent report published in Silence, Zheng and colleagues demonstrate a technique for robust and specific knockdown of miRNA expression in Caenorhabditis elegans using modified antisense oligonucleotides, which could be utilized as a powerful tool for the study of regulation and function of miRNAs in vivo.
MeSH term(s)	Animals ; Caenorhabditis elegans/genetics ; Cell Differentiation/genetics ; Conserved Sequence ; Gene Expression Regulation/drug effects ; Genome, Helminth/drug effects ; Longevity/genetics ; MicroRNAs/analysis ; MicroRNAs/antagonists & inhibitors ; MicroRNAs/metabolism ; MicroRNAs/physiology ; Oligonucleotides, Antisense/pharmacology ; RNA, Small Interfering/genetics
Chemical Substances	MicroRNAs ; Oligonucleotides, Antisense ; RNA, Small Interfering
Language	English
Publishing date	2010-04-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2082214-5
ISSN	1475-4924 ; 1475-4924
ISSN (online)	1475-4924
ISSN	1475-4924
DOI	10.1186/jbiol230
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Article ; Online: The microRNA-183/96/182 cluster inhibits lung cancer progression and metastasis by inducing an interleukin-2-mediated antitumor CD8

Kundu, Samrat T / Rodriguez, B Leticia / Gibson, Laura A / Warner, Amanda N / Perez, Mabel G / Bajaj, Rakhee / Fradette, Jared J / Class, Caleb A / Solis, Luisa M / Rojas Alvarez, Frank R / Wistuba, Ignacio I / Diao, Lixia / Chen, Fengju / Sachdeva, Mohit / Wang, Jing / Kirsch, David G / Creighton, Chad J / Gibbons, Don L

Genes & development

2022 Volume 36, Issue 9-10, Page(s) 582–600

Abstract: One of the mechanisms by which cancer cells acquire hyperinvasive and migratory properties with progressive loss of epithelial markers is the epithelial-to-mesenchymal transition (EMT). We have previously reported that in different cancer types, ... ...

Abstract	One of the mechanisms by which cancer cells acquire hyperinvasive and migratory properties with progressive loss of epithelial markers is the epithelial-to-mesenchymal transition (EMT). We have previously reported that in different cancer types, including nonsmall cell lung cancer (NSCLC), the microRNA-183/96/182 cluster (m96cl) is highly repressed in cells that have undergone EMT. In the present study, we used a novel conditional m96cl mouse to establish that loss of m96cl accelerated the growth of Kras mutant autochthonous lung adenocarcinomas. In contrast, ectopic expression of the m96cl in NSCLC cells results in a robust suppression of migration and invasion in vitro, and tumor growth and metastasis in vivo. Detailed immune profiling of the tumors revealed a significant enrichment of activated CD8
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/metabolism ; Cell Line, Tumor ; Interleukin-2/genetics ; Interleukin-2/metabolism ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; T-Lymphocytes, Cytotoxic ; Tumor Microenvironment
Chemical Substances	Interleukin-2 ; MicroRNAs
Language	English
Publishing date	2022-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.349321.121
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Zs.A 2292: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: TMEM106B drives lung cancer metastasis by inducing TFEB-dependent lysosome synthesis and secretion of cathepsins.

Kundu, Samrat T / Grzeskowiak, Caitlin L / Fradette, Jared J / Gibson, Laura A / Rodriguez, Leticia B / Creighton, Chad J / Scott, Kenneth L / Gibbons, Don L

Nature communications

2018 Volume 9, Issue 1, Page(s) 2731

Abstract: Metastatic lung cancer is the leading cause of cancer-associated mortality worldwide, therefore necessitating novel approaches to identify specific genetic drivers for lung cancer progression and metastasis. We recently performed an in vivo gain-of- ... ...

Abstract	Metastatic lung cancer is the leading cause of cancer-associated mortality worldwide, therefore necessitating novel approaches to identify specific genetic drivers for lung cancer progression and metastasis. We recently performed an in vivo gain-of-function genetic screen to identify driver genes of lung cancer metastasis. In the study reported here, we identify TMEM106B as a primary robust driver of lung cancer metastasis. Ectopic expression of TMEM106B could significantly promote the synthesis of enlarged vesicular lysosomes that are laden with elevated levels of active cathepsins. In a TFEB-dependent manner, TMEM106B could modulate the expression of lysosomal genes of the coordinated lysosomal expression and regulation (CLEAR) pathway in lung cancer cells and patient samples. We also demonstrate that TMEM106B-induced lysosomes undergo calcium-dependent exocytosis, thereby releasing active lysosomal cathepsins necessary for TMEM106B-mediated cancer cell invasion and metastasis in vivo, which could be therapeutically prevented by pharmacological inhibition of cathepsins. Further, in TCGA LUAD data sets, 19% of patients show elevated expression of TMEM106B, which predicts for poor disease-free and overall-survival.
MeSH term(s)	Adenocarcinoma of Lung/drug therapy ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/mortality ; Adenocarcinoma of Lung/pathology ; Animals ; Antineoplastic Agents/pharmacology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Calcium/metabolism ; Cathepsins/antagonists & inhibitors ; Cathepsins/genetics ; Cathepsins/metabolism ; Cell Line, Tumor ; Cysteine Proteinase Inhibitors/pharmacology ; Exocytosis ; Gene Expression Regulation, Neoplastic ; Humans ; Leucine/analogs & derivatives ; Leucine/pharmacology ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/mortality ; Lung Neoplasms/pathology ; Lysosomes/drug effects ; Lysosomes/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Neoplasm Metastasis ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Prognosis ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Proteolysis ; Signal Transduction ; Survival Analysis ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Cysteine Proteinase Inhibitors ; Membrane Proteins ; Nerve Tissue Proteins ; Protein Isoforms ; TFEB protein, human ; TMEM106B protein, human ; Cathepsins (EC 3.4.-) ; Leucine (GMW67QNF9C) ; aloxistatin (L5W337AOUR) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2018-07-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/s41467-018-05013-x
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Article: Lung cancer models reveal SARS-CoV-2-induced EMT contributes to COVID-19 pathophysiology.

Stewart, C Allison / Gay, Carl M / Ramkumar, Kavya / Cargill, Kasey R / Cardnell, Robert J / Nilsson, Monique B / Heeke, Simon / Park, Elizabeth M / Kundu, Samrat T / Diao, Lixia / Wang, Qi / Shen, Li / Xi, Yuanxin / Zhang, Bingnan / Della Corte, Carminia Maria / Fan, Youhong / Kundu, Kiran / Gao, Boning / Avila, Kimberley /

Pickering, Curtis R / Johnson, Faye M / Zhang, Jianjun / Kadara, Humam / Minna, John D / Gibbons, Don L / Wang, Jing / Heymach, John V / Byers, Lauren Averett

bioRxiv : the preprint server for biology

2021

Abstract: COVID-19 is an infectious disease caused by SARS-CoV-2, which enters host cells via the cell surface proteins ACE2 and TMPRSS2. Using a variety of normal and malignant models and tissues from the aerodigestive and respiratory tracts, we investigated the ... ...

Abstract	COVID-19 is an infectious disease caused by SARS-CoV-2, which enters host cells via the cell surface proteins ACE2 and TMPRSS2. Using a variety of normal and malignant models and tissues from the aerodigestive and respiratory tracts, we investigated the expression and regulation of
Keywords	covid19
Language	English
Publishing date	2021-01-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2020.05.28.122291
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Article ; Online: TMEM106B drives lung cancer metastasis by inducing TFEB-dependent lysosome synthesis and secretion of cathepsins

Samrat T. Kundu / Caitlin L. Grzeskowiak / Jared J. Fradette / Laura A. Gibson / Leticia B. Rodriguez / Chad J. Creighton / Kenneth L. Scott / Don L. Gibbons

Nature Communications, Vol 9, Iss 1, Pp 1-

2018 Volume 16

Abstract: One of the major causes of cancer-related mortality is represented by metastatic lung cancer. Here the authors characterize the role of TMEM106B in driving metastatic lung adenocarcinoma and suggest that TMEM106B-mediated secretion of cathespin impacts ... ...

Abstract	One of the major causes of cancer-related mortality is represented by metastatic lung cancer. Here the authors characterize the role of TMEM106B in driving metastatic lung adenocarcinoma and suggest that TMEM106B-mediated secretion of cathespin impacts cell migration and invasion of lung cancer cells, increasing metastatic spreading.
Keywords	Science ; Q
Language	English
Publishing date	2018-07-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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