LIVIVO - Search results -

Search results

Result 1 - 10 of total 12

Search options

Article ; Online: Single-cell RNA sequencing of a new transgenic t(8;21) preleukemia mouse model reveals regulatory networks promoting leukemic transformation.

Yan, Ming / Liu, Mengdan / Davis, Amanda G / Stoner, Samuel A / Zhang, Dong-Er

2023 Volume 38, Issue 1, Page(s) 31–44

Abstract: T(8;21)(q22;q22), which generates the AML1-ETO fusion oncoprotein, is a common chromosomal abnormality in acute myeloid leukemia (AML) patients. Despite having favorable prognosis, 40% of patients will relapse, highlighting the need for innovative models ...

Abstract	T(8;21)(q22;q22), which generates the AML1-ETO fusion oncoprotein, is a common chromosomal abnormality in acute myeloid leukemia (AML) patients. Despite having favorable prognosis, 40% of patients will relapse, highlighting the need for innovative models and application of the newest technologies to study t(8;21) leukemogenesis. Currently, available AML1-ETO mouse models have limited utility for studying the pre-leukemic stage because AML1-ETO produces mild hematopoietic phenotypes and no leukemic transformation. Conversely, overexpression of a truncated variant, AML1-ETO9a (AE9a), promotes fully penetrant leukemia and is too potent for studying pre-leukemic changes. To overcome these limitations, we devised a germline-transmitted Rosa26 locus AE9a knock-in mouse model that moderately overexpressed AE9a and developed leukemia with long latency and low penetrance. We observed pre-leukemic alterations in AE9a mice, including skewing of progenitors towards granulocyte/monocyte lineages and replating of stem and progenitor cells. Next, we performed single-cell RNA sequencing to identify specific cell populations that contribute to these pre-leukemic phenotypes. We discovered a subset of common myeloid progenitors that have heightened granulocyte/monocyte bias in AE9a mice. We also observed dysregulation of key hematopoietic transcription factor target gene networks, blocking cellular differentiation. Finally, we identified Sox4 activation as a potential contributor to stem cell self-renewal during the pre-leukemic stage.
MeSH term(s)	Humans ; Mice ; Animals ; Preleukemia ; RUNX1 Translocation Partner 1 Protein/genetics ; Leukemia, Myeloid, Acute/genetics ; Core Binding Factor Alpha 2 Subunit/genetics ; Animals, Genetically Modified ; Sequence Analysis, RNA ; Oncogene Proteins, Fusion/genetics
Chemical Substances	RUNX1 Translocation Partner 1 Protein ; Core Binding Factor Alpha 2 Subunit ; Oncogene Proteins, Fusion
Language	English
Publishing date	2023-10-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-023-02063-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2295: 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)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: Expansion of interferon inducible gene pool via USP18 inhibition promotes cancer cell pyroptosis.

Arimoto, Kei-Ichiro / Miyauchi, Sayuri / Troutman, Ty D / Zhang, Yue / Liu, Mengdan / Stoner, Samuel A / Davis, Amanda G / Fan, Jun-Bao / Huang, Yi-Jou / Yan, Ming / Glass, Christopher K / Zhang, Dong-Er

Nature communications

2023 Volume 14, Issue 1, Page(s) 251

Abstract: While immunotherapy has emerged as a breakthrough cancer therapy, it is only effective in some patients, indicating the need of alternative therapeutic strategies. Induction of cancer immunogenic cell death (ICD) is one promising way to elicit potent ... ...

Abstract	While immunotherapy has emerged as a breakthrough cancer therapy, it is only effective in some patients, indicating the need of alternative therapeutic strategies. Induction of cancer immunogenic cell death (ICD) is one promising way to elicit potent adaptive immune responses against tumor-associated antigens. Type I interferon (IFN) is well known to play important roles in different aspects of immune responses, including modulating ICD in anti-tumor action. However, how to expand IFN effect in promoting ICD responses has not been addressed. Here we show that depletion of ubiquitin specific protease 18 (USP18), a negative regulator of IFN signaling, selectively induces cancer cell ICD. Lower USP18 expression correlates with better survival across human selected cancer types and delays cancer progression in mouse models. Mechanistically, nuclear USP18 controls the enhancer landscape of cancer cells and diminishes STAT2-mediated transcription complex binding to IFN-responsive elements. Consequently, USP18 suppression not only enhances expression of canonical IFN-stimulated genes (ISGs), but also activates the expression of a set of atypical ISGs and NF-κB target genes, including genes such as Polo like kinase 2 (PLK2), that induce cancer pyroptosis. These findings may support the use of targeting USP18 as a potential cancer immunotherapy.
MeSH term(s)	Mice ; Animals ; Humans ; Pyroptosis ; Gene Pool ; Signal Transduction ; NF-kappa B/metabolism ; Interferon Type I/genetics ; Ubiquitin Thiolesterase/metabolism ; Neoplasms/genetics
Chemical Substances	NF-kappa B ; Interferon Type I ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; USP18 protein, human (EC 3.4.19.12)
Language	English
Publishing date	2023-01-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-35348-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A trigger channel threshold artifact in nanoparticle analysis.

Nolan, John P / Stoner, Samuel A

Cytometry. Part A : the journal of the International Society for Analytical Cytology

2013 Volume 83, Issue 3, Page(s) 301–305

Abstract: The analysis of individual nanoparticles by flow cytometry involves the measurement of dim signals that are near the detection limits of the instrument. Discriminating the signal from particles of interest from that of background particles in buffers and ...

Abstract	The analysis of individual nanoparticles by flow cytometry involves the measurement of dim signals that are near the detection limits of the instrument. Discriminating the signal from particles of interest from that of background particles in buffers and from optical and electronic noise can be challenging, and requires careful consideration of the measurement approach, control experiments, and scrutiny of the resulting data. In applying this scrutiny, we have come to recognize an artifact that results from the inappropriate selection of the trigger channel threshold that might not be obvious to the casual user. When measuring dim signals close to the noise or background levels, it is intuitive and common for the operator to adjust the trigger threshold to minimize the "false triggers" acquired by the system, and then to run the unknown sample, interpreting the events detected above the background as measurements of individual particles. We show here that when this approach is used to measure particles whose signals fall below the trigger threshold, only coincident events are detected, producing erroneous measurements of both particle number and brightness. We suggest that in many cases, the analysis of dim nanoparticles is best achieved using a fluorescence channel for the trigger.
MeSH term(s)	Artifacts ; Flow Cytometry/instrumentation ; Flow Cytometry/methods ; Fluorescence ; Limit of Detection ; Nanoparticles/analysis ; Signal-To-Noise Ratio
Language	English
Publishing date	2013-01-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2099868-5
ISSN	1552-4930 ; 0196-4763 ; 1552-4922
ISSN (online)	1552-4930
ISSN	0196-4763 ; 1552-4922
DOI	10.1002/cyto.a.22255
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1688: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 68: Show issues

Order via subito

Details ▾

Article ; Online: Sex chromosome loss and the pseudoautosomal region genes in hematological malignancies.

Weng, Stephanie / Stoner, Samuel A / Zhang, Dong-Er

Oncotarget

2016 Volume 7, Issue 44, Page(s) 72356–72372

Abstract: Cytogenetic aberrations, such as chromosomal translocations, aneuploidy, and amplifications, are frequently detected in hematological malignancies. For many of the common autosomal aberrations, the mechanisms underlying their roles in cancer development ... ...

Abstract	Cytogenetic aberrations, such as chromosomal translocations, aneuploidy, and amplifications, are frequently detected in hematological malignancies. For many of the common autosomal aberrations, the mechanisms underlying their roles in cancer development have been well-characterized. On the contrary, although loss of a sex chromosome is observed in a broad range of hematological malignancies, how it cooperates in disease development is less understood. Nevertheless, it has been postulated that tumor suppressor genes reside on the sex chromosomes. Although the X and Y sex chromosomes are highly divergent, the pseudoautosomal regions are homologous between both chromosomes. Here, we review what is currently known about the pseudoautosomal region genes in the hematological system. Additionally, we discuss implications for haploinsufficiency of critical pseudoautosomal region sex chromosome genes, driven by sex chromosome loss, in promoting hematological malignancies. Because mechanistic studies on disease development rely heavily on murine models, we also discuss the challenges and caveats of existing models, and propose alternatives for examining the involvement of pseudoautosomal region genes and loss of a sex chromosome in vivo. With the widespread detection of loss of a sex chromosome in different hematological malignances, the elucidation of the role of pseudoautosomal region genes in the development and progression of these diseases would be invaluable to the field.
Language	English
Publishing date	2016-11-01
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.12050
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Negative regulation of type I IFN signaling.

Arimoto, Kei-Ichiro / Miyauchi, Sayuri / Stoner, Samuel A / Fan, Jun-Bao / Zhang, Dong-Er

Journal of leukocyte biology

2018

Abstract: Type I IFNs (α, β, and others) are a family of cytokines that are produced in physiological conditions as well as in response to the activation of pattern recognition receptors. They are critically important in controlling the host innate and adaptive ... ...

Abstract	Type I IFNs (α, β, and others) are a family of cytokines that are produced in physiological conditions as well as in response to the activation of pattern recognition receptors. They are critically important in controlling the host innate and adaptive immune response to viral and some bacterial infections, cancer, and other inflammatory stimuli. However, dysregulation of type I IFN production or response can contribute to immune pathologies termed "interferonopathies", pointing to the importance of balanced activating signals with tightly regulated mechanisms of tuning this signaling. Here, we summarize the recent advances of how type I IFN production and response are controlled at multiple levels of the type I IFN signaling cascade.
Language	English
Publishing date	2018-01-22
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.2MIR0817-342R
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 603: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Alternative polyadenylation dysregulation contributes to the differentiation block of acute myeloid leukemia.

Davis, Amanda G / Johnson, Daniel T / Zheng, Dinghai / Wang, Ruijia / Jayne, Nathan D / Liu, Mengdan / Shin, Jihae / Wang, Luyang / Stoner, Samuel A / Zhou, Jie-Hua / Ball, Edward D / Tian, Bin / Zhang, Dong-Er

Blood

2021 Volume 139, Issue 3, Page(s) 424–438

Abstract: Posttranscriptional regulation has emerged as a driver for leukemia development and an avenue for therapeutic targeting. Among posttranscriptional processes, alternative polyadenylation (APA) is globally dysregulated across cancer types. However, limited ...

Abstract	Posttranscriptional regulation has emerged as a driver for leukemia development and an avenue for therapeutic targeting. Among posttranscriptional processes, alternative polyadenylation (APA) is globally dysregulated across cancer types. However, limited studies have focused on the prevalence and role of APA in myeloid leukemia. Furthermore, it is poorly understood how altered poly(A) site usage of individual genes contributes to malignancy or whether targeting global APA patterns might alter oncogenic potential. In this study, we examined global APA dysregulation in patients with acute myeloid leukemia (AML) by performing 3' region extraction and deep sequencing (3'READS) on a subset of AML patient samples along with healthy hematopoietic stem and progenitor cells (HSPCs) and by analyzing publicly available data from a broad AML patient cohort. We show that patient cells exhibit global 3' untranslated region (UTR) shortening and coding sequence lengthening due to differences in poly(A) site (PAS) usage. Among APA regulators, expression of FIP1L1, one of the core cleavage and polyadenylation factors, correlated with the degree of APA dysregulation in our 3'READS data set. Targeting global APA by FIP1L1 knockdown reversed the global trends seen in patients. Importantly, FIP1L1 knockdown induced differentiation of t(8;21) cells by promoting 3'UTR lengthening and downregulation of the fusion oncoprotein AML1-ETO. In non-t(8;21) cells, FIP1L1 knockdown also promoted differentiation by attenuating mechanistic target of rapamycin complex 1 (mTORC1) signaling and reducing MYC protein levels. Our study provides mechanistic insights into the role of APA in AML pathogenesis and indicates that targeting global APA patterns can overcome the differentiation block in patients with AML.
MeSH term(s)	3' Untranslated Regions ; Cells, Cultured ; Gene Expression Regulation, Leukemic ; Hematopoietic Stem Cells/metabolism ; Humans ; Leukemia, Myeloid, Acute/genetics ; Polyadenylation ; Tumor Cells, Cultured ; mRNA Cleavage and Polyadenylation Factors/genetics
Chemical Substances	3' Untranslated Regions ; FIP1L1 protein, human ; mRNA Cleavage and Polyadenylation Factors
Language	English
Publishing date	2021-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2020005693
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 364: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The RUNX1-ETO target gene RASSF2 suppresses t(8;21) AML development and regulates Rac GTPase signaling.

Stoner, Samuel A / Liu, Katherine Tin Heng / Andrews, Elizabeth T / Liu, Mengdan / Arimoto, Kei-Ichiro / Yan, Ming / Davis, Amanda G / Weng, Stephanie / Dow, Michelle / Xian, Su / DeKelver, Russell C / Carter, Hannah / Zhang, Dong-Er

Blood cancer journal

2020 Volume 10, Issue 2, Page(s) 16

Abstract: Large-scale chromosomal translocations are frequent oncogenic drivers in acute myeloid leukemia (AML). These translocations often occur in critical transcriptional/epigenetic regulators and contribute to malignant cell growth through alteration of normal ...

Abstract	Large-scale chromosomal translocations are frequent oncogenic drivers in acute myeloid leukemia (AML). These translocations often occur in critical transcriptional/epigenetic regulators and contribute to malignant cell growth through alteration of normal gene expression. Despite this knowledge, the specific gene expression alterations that contribute to the development of leukemia remain incompletely understood. Here, through characterization of transcriptional regulation by the RUNX1-ETO fusion protein, we have identified Ras-association domain family member 2 (RASSF2) as a critical gene that is aberrantly transcriptionally repressed in t(8;21)-associated AML. Re-expression of RASSF2 specifically inhibits t(8;21) AML development in multiple models. Through biochemical and functional studies, we demonstrate RASSF2-mediated functions to be dependent on interaction with Hippo kinases, MST1 and MST2, but independent of canonical Hippo pathway signaling. Using proximity-based biotin labeling we define the RASSF2-proximal proteome in leukemia cells and reveal association with Rac GTPase-related proteins, including an interaction with the guanine nucleotide exchange factor, DOCK2. Importantly, RASSF2 knockdown impairs Rac GTPase activation, and RASSF2 expression is broadly correlated with Rac-mediated signal transduction in AML patients. Together, these data reveal a previously unappreciated mechanistic link between RASSF2, Hippo kinases, and Rac activity with potentially broad functional consequences in leukemia.
MeSH term(s)	Animals ; Biomarkers, Tumor/genetics ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Human, Pair 8/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; Leukemia, Myeloid, Acute/prevention & control ; Mice ; Mice, Inbred C57BL ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Translocation, Genetic ; Tumor Cells, Cultured ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Xenograft Model Antitumor Assays ; rac GTP-Binding Proteins/genetics ; rac GTP-Binding Proteins/metabolism
Chemical Substances	Biomarkers, Tumor ; Oncogene Proteins, Fusion ; RASSF2 protein, human ; RUNX1-IT1 long non-coding RNA, human ; Tumor Suppressor Proteins ; rac GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2020-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2600560-8
ISSN	2044-5385 ; 2044-5385
ISSN (online)	2044-5385
ISSN	2044-5385
DOI	10.1038/s41408-020-0282-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Hippo kinase loss contributes to del(20q) hematologic malignancies through chronic innate immune activation.

Stoner, Samuel A / Yan, Ming / Liu, Katherine Tin Heng / Arimoto, Kei-Ichiro / Shima, Takahiro / Wang, Huan-You / Johnson, Daniel T / Bejar, Rafael / Jamieson, Catriona / Guan, Kun-Liang / Zhang, Dong-Er

Blood

2019 Volume 134, Issue 20, Page(s) 1730–1744

Abstract: Heterozygous deletions within chromosome 20q, or del(20q), are frequent cytogenetic abnormalities detected in hematologic malignancies. To date, identification of genes in the del(20q) common deleted region that contribute to disease development have ... ...

Abstract	Heterozygous deletions within chromosome 20q, or del(20q), are frequent cytogenetic abnormalities detected in hematologic malignancies. To date, identification of genes in the del(20q) common deleted region that contribute to disease development have remained elusive. Through assessment of patient gene expression, we have identified STK4 (encoding Hippo kinase MST1) as a 20q gene that is downregulated below haploinsufficient amounts in myelodysplastic syndrome (MDS) and myeloproliferative neoplasm (MPN). Hematopoietic-specific gene inactivation in mice revealed Hippo kinase loss to induce splenomegaly, thrombocytopenia, megakaryocytic dysplasia, and a propensity for chronic granulocytosis; phenotypes that closely resemble those observed in patients harboring del(20q). In a JAK2-V617F model, heterozygous Hippo kinase inactivation led to accelerated development of lethal myelofibrosis, recapitulating adverse MPN disease progression and revealing a novel genetic interaction between these 2 molecular events. Quantitative serum protein profiling showed that myelofibrotic transformation in mice was associated with cooperative effects of JAK2-V617F and Hippo kinase inactivation on innate immune-associated proinflammatory cytokine production, including IL-1β and IL-6. Mechanistically, MST1 interacted with IRAK1, and shRNA-mediated knockdown was sufficient to increase IRAK1-dependent innate immune activation of NF-κB in human myeloid cells. Consistent with this, treatment with a small molecule IRAK1/4 inhibitor rescued the aberrantly elevated IL-1β production in the JAK2-V617F MPN model. This study identified Hippo kinase MST1 (STK4) as having a central role in the biology of del(20q)-associated hematologic malignancies and revealed a novel molecular basis of adverse MPN progression that may be therapeutically exploitable via IRAK1 inhibition.
MeSH term(s)	Animals ; Chromosome Deletion ; Chromosomes, Human, Pair 20/genetics ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Hematologic Neoplasms/genetics ; Hematologic Neoplasms/immunology ; Humans ; Immunity, Innate ; Intracellular Signaling Peptides and Proteins ; Mice ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/immunology ; Myeloproliferative Disorders/genetics ; Myeloproliferative Disorders/immunology ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/immunology
Chemical Substances	Intracellular Signaling Peptides and Proteins ; Stk4 protein, mouse (EC 2.7.1.-) ; STK4 protein, human (EC 2.7.1.11) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2019-09-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2019000170
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 364: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: High sensitivity flow cytometry of membrane vesicles.

Stoner, Samuel A / Duggan, Erika / Condello, Danilo / Guerrero, Abraham / Turk, James R / Narayanan, Padma K / Nolan, John P

Cytometry. Part A : the journal of the International Society for Analytical Cytology

2016 Volume 89, Issue 2, Page(s) 196–206

Abstract: Extracellular vesicles (EVs) are attracting attention as vehicles for inter-cellular signaling that may have value as diagnostic or therapeutic targets. EVs are released by many cell types and by different mechanisms, resulting in phenotypic ... ...

Abstract	Extracellular vesicles (EVs) are attracting attention as vehicles for inter-cellular signaling that may have value as diagnostic or therapeutic targets. EVs are released by many cell types and by different mechanisms, resulting in phenotypic heterogeneity that makes them a challenge to study. Flow cytometry is a popular tool for characterizing heterogeneous mixtures of particles such as cell types within blood, but the small size of EVs makes them difficult to measure using conventional flow cytometry. To address this limitation, a high sensitivity flow cytometer was constructed and EV measurement approaches that allowed them to enumerate and estimate the size of individual EVs, as well as measure the presence of surface markers to identify phenotypic subsets of EVs. Several fluorescent membrane probes were evaluated and it was found that the voltage sensing dye di-8-ANEPPS could produce vesicle fluorescence in proportion to vesicle surface area, allowing for accurate measurements of EV number and size. Fluorescence-labeled annexin V and anti-CD61 antibody was used to measure the abundance of these surface markers on EVs in rat plasma. It was shown that treatment of platelet rich plasma with calcium ionophore resulted in an increase in the fraction of annexin V and CD61-positive EVs. Vesicle flow cytometry using fluorescence-based detection of EVs has the potential to realize the potential of cell-derived membrane vesicles as functional biomarkers for a variety of applications.
MeSH term(s)	Animals ; Calibration ; Extracellular Vesicles/chemistry ; Extracellular Vesicles/physiology ; Female ; Flow Cytometry/methods ; Flow Cytometry/standards ; Limit of Detection ; Platelet-Rich Plasma/chemistry ; Rats, Sprague-Dawley ; Staining and Labeling
Language	English
Publishing date	2016-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2099868-5
ISSN	1552-4930 ; 0196-4763 ; 1552-4922
ISSN (online)	1552-4930
ISSN	0196-4763 ; 1552-4922
DOI	10.1002/cyto.a.22787
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1688: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 68: Show issues

Order via subito

Details ▾

Article: Single cell analysis using surface enhanced Raman scattering (SERS) tags

Nolan, John P / Duggan, Erika / Liu, Er / Condello, Danilo / Dave, Isha / Stoner, Samuel A

Methods. 2012 July, v. 57, no. 3

2012

Abstract: Fluorescence is a mainstay of bioanalytical methods, offering sensitive and quantitative reporting, often in multiplexed or multiparameter assays. Perhaps the best example of the latter is flow cytometry, where instruments equipped with multiple lasers ... ...

Abstract	Fluorescence is a mainstay of bioanalytical methods, offering sensitive and quantitative reporting, often in multiplexed or multiparameter assays. Perhaps the best example of the latter is flow cytometry, where instruments equipped with multiple lasers and detectors allow measurement of 15 or more different fluorophores simultaneously, but increases beyond this number are limited by the relatively broad emission spectra. Surface enhanced Raman scattering (SERS) from metal nanoparticles can produce signal intensities that rival fluorescence, but with narrower spectral features that allow a greater degree of multiplexing. We are developing nanoparticle SERS tags as well as Raman flow cytometers for multiparameter single cell analysis of suspension or adherent cells. SERS tags are based on plasmonically active nanoparticles (gold nanorods) whose plasmon resonance can be tuned to give optimal SERS signals at a desired excitation wavelength. Raman resonant compounds are adsorbed on the nanoparticles to confer a unique spectral fingerprint on each SERS tag, which are then encapsulated in a polymer coating for conjugation to antibodies or other targeting molecules. Raman flow cytometry employs a high resolution spectral flow cytometer capable of measuring the complete SERS spectra, as well as conventional flow cytometry measurements, from thousands of individual cells per minute. Automated spectral unmixing algorithms extract the contributions of each SERS tag from each cell to generate high content, multiparameter single cell population data. SERS-based cytometry is a powerful complement to conventional fluorescence-based cytometry. The narrow spectral features of the SERS signal enables more distinct probes to be measured in a smaller region of the optical spectrum with a single laser and detector, allowing for higher levels of multiplexing and multiparameter analysis.
Keywords	Raman spectroscopy ; algorithms ; antibodies ; coatings ; complement ; detectors ; flow cytometry ; fluorescence ; fluorescent dyes ; gold ; lasers ; nanoparticles ; nanorods ; polymers ; spectral analysis ; wavelengths
Language	English
Dates of publication	2012-07
Size	p. 272-279.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1066584-5
ISSN	1095-9130 ; 1046-2023
ISSN (online)	1095-9130
ISSN	1046-2023
DOI	10.1016/j.ymeth.2012.03.024
Database	NAL-Catalogue (AGRICOLA)

In stock of ZB MED Cologne/Königswinter

Zs.A 3239: 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)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito