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Article ; Online: Molecular Mechnisms of Liver-Specific Albumin and α-Fetoprotein Gene Regulation: A Review: albumin gene/α-fetoprotein gene/regulation promoter/liver-specific.

Papaconstantinou, John / Rabek, Jeffrey P / Zhang, Dong-Er

2023 Volume 32, Issue 2, Page(s) 205–216

Language	English
Publishing date	2023-06-06
Publishing country	Japan
Document type	Journal Article
ZDB-ID	280433-5
ISSN	1440-169X ; 0012-1592
ISSN (online)	1440-169X
ISSN	0012-1592
DOI	10.1111/j.1440-169X.1990.00205.x
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Article ; Online: Reprogramming of tumor-associated macrophages via NEDD4-mediated CSF1R degradation by targeting USP18.

Miyauchi, Sayuri / Arimoto, Kei-Ichiro / Liu, Mengdan / Zhang, Yue / Zhang, Dong-Er

Cell reports

2023 Volume 42, Issue 12, Page(s) 113560

Abstract: Tumor-associated myeloid cells modulate the tumor microenvironment and affect tumor progression. Type I interferon (IFN-I) has multiple effects on tumors and immune response, and ubiquitin-specific peptidase 18 (USP18) functions as a negative regulator ... ...

Abstract	Tumor-associated myeloid cells modulate the tumor microenvironment and affect tumor progression. Type I interferon (IFN-I) has multiple effects on tumors and immune response, and ubiquitin-specific peptidase 18 (USP18) functions as a negative regulator of IFN-I signal transduction. This study aims to examine the function of IFN-I in myeloid cells during tumor progression. Here, we show that deletion of USP18 in myeloid cells suppresses tumor progression. Enhanced IFN-I signaling and blocked USP18 expression prompt downregulation of colony stimulating factor 1 receptor (CSF1R) and polarization of tumor-associated macrophages toward pro-inflammatory phenotypes. Further in vitro experiments reveal that downregulation of CSF1R is mediated by ubiquitin-proteasome degradation via E3 ligase neural precursor cell-expressed, developmentaly downregulated 4 (NEDD4) and the IFN-induced increase in ubiquitin E2 ubiquitin-conjugating enzyme H5. USP18 impairs ubiquitination and subsequent degradation of CSF1R by interrupting NEDD4 binding to CSF1R. These results reveal a previously unappreciated role of IFN-I in macrophage polarization by regulating CSF1R via USP18 and suggest targeting USP18 in myeloid-lineage cells as an effective strategy for IFN-based therapies.
MeSH term(s)	Tumor-Associated Macrophages ; Signal Transduction ; Receptor Protein-Tyrosine Kinases ; Ubiquitin ; Ubiquitination
Chemical Substances	Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Ubiquitin
Language	English
Publishing date	2023-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113560
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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

Leukemia

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
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Article: Chromatin-associated RNA Dictates the ecDNA Interactome in the Nucleus.

Liang, Zhengyu / Gilbreath, Collin / Liu, Wenyue / Wang, Yan / Zhang, Michael Q / Zhang, Dong-Er / Wu, Sihan / Fu, Xiang-Dong

bioRxiv : the preprint server for biology

2023

Abstract: Extrachromosomal DNA (ecDNA) promotes cancer by driving copy number heterogeneity and amplifying oncogenes along with functional enhancers. More recent studies suggest two additional mechanisms for further enhancing their oncogenic potential, one via ... ...

Abstract	Extrachromosomal DNA (ecDNA) promotes cancer by driving copy number heterogeneity and amplifying oncogenes along with functional enhancers. More recent studies suggest two additional mechanisms for further enhancing their oncogenic potential, one via forming ecDNA hubs to augment oncogene expression
Language	English
Publishing date	2023-07-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.27.550855
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Article ; Online: RUNX1 C-terminal Mutations Impair Blood Cell Differentiation by Perturbing Specific Enhancer-Promoter Networks.

Jayne, Nathan Daniel / Liang, Zhengyu / Lim, Do-Hwan / Chen, Poshen Benson / Diaz, Cristina / Arimoto, Kei-Ichiro / Xia, Lingbo / Liu, Mengdan / Ren, Bing / Fu, Xiang-Dong / Zhang, Dong-Er

Blood advances

2024

Abstract: The transcription factor RUNX1 is a master regulator of hematopoiesis and is frequently mutated in myeloid malignancies. Mutations in its runt homology domain (RHD) frequently disrupt DNA binding and result in loss of RUNX1 function. However, it is not ... ...

Abstract	The transcription factor RUNX1 is a master regulator of hematopoiesis and is frequently mutated in myeloid malignancies. Mutations in its runt homology domain (RHD) frequently disrupt DNA binding and result in loss of RUNX1 function. However, it is not clearly understood how other RUNX1 mutations contribute to disease development. Here, we characterize RUNX1 mutations outside of the RHD. Our analysis of patient datasets revealed that mutations within the C-terminus frequently occur in hematopoietic disorders. Remarkably, most of these mutations were nonsense or frameshift and predicted to be exempt from nonsense mediated mRNA decay. Therefore, this class of mutation is projected to produce DNA-binding proteins that contribute to pathogenesis in a distinct manner. To model this, we introduced the RUNX1R320* mutation into the endogenous gene locus and demonstrated the production of RUNX1R320* protein. Expression of RUNX1R320* resulted in the disruption of RUNX1 regulated processes such as megakaryocytic differentiation through a transcriptional signature different from RUNX1 depletion. To understand the underlying mechanisms, we utilized Global RNA Interactions with DNA by deep sequencing (GRID-seq) to examine enhancer-promoter connections. We identified wide-spread alteration of enhancer-promoter networks within RUNX1 mutant cells. Additionally, we uncovered enrichment of RUNX1R320* and FOXK2 binding at the MYC super enhancer locus, significantly upregulating MYC transcription and signaling pathways. Together, our study demonstrates that most RUNX1 mutations outside the DNA binding domain are not subject to nonsense mediated decay, producing protein products that act in concert with additional cofactors to dysregulate hematopoiesis through mechanisms distinct from that induced by RUNX1 depletion.
Language	English
Publishing date	2024-03-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023011484
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Article: ZetaSuite: computational analysis of two-dimensional high-throughput data from multi-target screens and single-cell transcriptomics

Hao, Yajing / Zhang, Shuyang / Shao, Changwei / Li, Junhui / Zhao, Guofeng / Zhang, Dong-Er / Fu, Xiang-Dong

Genome biology. 2022 Dec., v. 23, no. 1

2022

Abstract: Two-dimensional high-throughput data have become increasingly common in functional genomics studies, which raises new challenges in data analysis. Here, we introduce a new statistic called Zeta, initially developed to identify global splicing regulators ... ...

Abstract	Two-dimensional high-throughput data have become increasingly common in functional genomics studies, which raises new challenges in data analysis. Here, we introduce a new statistic called Zeta, initially developed to identify global splicing regulators from a two-dimensional RNAi screen, a high-throughput screen coupled with high-throughput functional readouts, and ZetaSuite, a software package to facilitate general application of the Zeta statistics. We compare our approach with existing methods using multiple benchmarked datasets and then demonstrate the broad utility of ZetaSuite in processing public data from large-scale cancer dependency screens and single-cell transcriptomics studies to elucidate novel biological insights.
Keywords	computer software ; data collection ; genome ; genomics ; statistics ; transcriptomics
Language	English
Dates of publication	2022-12
Size	p. 162.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-022-02729-4
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Article: MicroRNA let-7b downregulates AML1-ETO oncogene expression in t(8;21) AML by targeting its 3'UTR.

Johnson, Daniel T / Davis, Amanda G / Zhou, Jie-Hua / Ball, Edward D / Zhang, Dong-Er

Experimental hematology & oncology

2021 Volume 10, Issue 1, Page(s) 8

Abstract: Background: Acute myeloid leukemia (AML) with the t(8;21)(q22;q22) chromosomal translocation is among the most common subtypes of AML and produces the AML1-ETO (RUNX1-ETO, RUNX1-RUNX1T1) oncogenic fusion gene. AML1-ETO functions as an aberrant ... ...

Abstract	Background: Acute myeloid leukemia (AML) with the t(8;21)(q22;q22) chromosomal translocation is among the most common subtypes of AML and produces the AML1-ETO (RUNX1-ETO, RUNX1-RUNX1T1) oncogenic fusion gene. AML1-ETO functions as an aberrant transcription factor which plays a key role in blocking normal hematopoiesis. Thus, the expression of AML1-ETO is critical to t(8;21) AML leukemogenesis and maintenance. Post-transcriptional regulation of gene expression is often mediated through interactions between trans-factors and cis-elements within transcript 3'-untranslated regions (UTR). AML1-ETO uses the 3'UTR of the ETO gene, which is not normally expressed in hematopoietic cells. Therefore, the mechanisms regulating AML1-ETO expression via the 3'UTR are attractive therapeutic targets. Methods: We used RNA-sequencing of t(8;21) patients and cell lines to examine the 3'UTR isoforms used by AML1-ETO transcripts. Using luciferase assay approaches, we test the relative contribution of 3'UTR cis elements to AML1-ETO expression. We further use let-7b microRNA mimics and anti-let-7b sponges for functional studies of t(8;21) AML cell lines. Results: In this study, we examine the regulation of AML1-ETO via the 3'UTR. We demonstrate that AML1-ETO transcripts primarily use a 3.7 kb isoform of the ETO 3'UTR in both t(8;21) patients and cell lines. We identify a negative regulatory element within the AML1-ETO 3'UTR. We further demonstrate that the let-7b microRNA directly represses AML1-ETO through this site. Finally, we find that let-7b inhibits the proliferation of t(8;21) AML cell lines, rescues expression of AML1-ETO target genes, and promotes differentiation. Conclusions: AML1-ETO is post-transcriptionally regulated by let-7b, which contributes to the leukemic phenotype of t(8;21) AML and may be important for t(8;21) leukemogenesis and maintenance.
Language	English
Publishing date	2021-02-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2669066-4
ISSN	2162-3619
ISSN	2162-3619
DOI	10.1186/s40164-021-00204-7
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Article ; Online: C11orf21

Matsumoto, Akifumi / Yoshida, Tatsushi / Shima, Takahiro / Yamasaki, Kenta / Tadagaki, Kenjiro / Kondo, Noriko / Kuwahara, Yasumichi / Zhang, Dong-Er / Okuda, Tsukasa

BBA advances

2022 Volume 2, Page(s) 100047

Abstract: The fusion protein RUNX1-ETO is an oncogenic transcription factor generated by t(8;21) chromosome translocation, which is found in FAB-M2-type acute myeloid leukemia (AML). RUNX1-ETO is known to dysregulate the normal RUNX1 transcriptional network, which ...

Abstract	The fusion protein RUNX1-ETO is an oncogenic transcription factor generated by t(8;21) chromosome translocation, which is found in FAB-M2-type acute myeloid leukemia (AML). RUNX1-ETO is known to dysregulate the normal RUNX1 transcriptional network, which should involve essential factors for the onset of AML with t(8;21). In this study, we screened for possible transcriptional targets of RUNX1 by reanalysis of public data
Language	English
Publishing date	2022-02-25
Publishing country	Netherlands
Document type	Journal Article
ISSN	2667-1603
ISSN (online)	2667-1603
DOI	10.1016/j.bbadva.2022.100047
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Article ; Online: ZetaSuite: computational analysis of two-dimensional high-throughput data from multi-target screens and single-cell transcriptomics.

Hao, Yajing / Zhang, Shuyang / Shao, Changwei / Li, Junhui / Zhao, Guofeng / Zhang, Dong-Er / Fu, Xiang-Dong

Genome biology

2022 Volume 23, Issue 1, Page(s) 162

Abstract	Two-dimensional high-throughput data have become increasingly common in functional genomics studies, which raises new challenges in data analysis. Here, we introduce a new statistic called Zeta, initially developed to identify global splicing regulators from a two-dimensional RNAi screen, a high-throughput screen coupled with high-throughput functional readouts, and ZetaSuite, a software package to facilitate general application of the Zeta statistics. We compare our approach with existing methods using multiple benchmarked datasets and then demonstrate the broad utility of ZetaSuite in processing public data from large-scale cancer dependency screens and single-cell transcriptomics studies to elucidate novel biological insights.
MeSH term(s)	Genomics/methods ; High-Throughput Screening Assays/methods ; RNA Interference ; Single-Cell Analysis ; Software ; Transcriptome
Language	English
Publishing date	2022-07-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-022-02729-4
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Article: C11orf21, a novel RUNX1 target gene, is down-regulated by RUNX1-ETO

Matsumoto, Akifumi / Yoshida, Tatsushi / Shima, Takahiro / Yamasaki, Kenta / Tadagaki, Kenjiro / Kondo, Noriko / Kuwahara, Yasumichi / Zhang, Dong-Er / Okuda, Tsukasa

BBA advances. 2022, v. 2

2022

Abstract	The fusion protein RUNX1-ETO is an oncogenic transcription factor generated by t(8;21) chromosome translocation, which is found in FAB-M2-type acute myeloid leukemia (AML). RUNX1-ETO is known to dysregulate the normal RUNX1 transcriptional network, which should involve essential factors for the onset of AML with t(8;21). In this study, we screened for possible transcriptional targets of RUNX1 by reanalysis of public data in silico, and identified C11orf21 as a novel RUNX1 target gene because its expression was down-regulated in the presence of RUNX1-ETO. The expression level of C11orf21 was low in AML patient samples with t(8;21) and in Kasumi-1 cells, which carry RUNX1-ETO. Knockdown of RUNX1-ETO in Kasumi-1 cells restored C11orf21 expression, whereas overexpression of RUNX1 up-regulated C11orf21 expression. In addition, knockdown of RUNX1 in other human leukemia cells without RUNX-ETO, such as K562, led to a decrease in C11orf21 expression. Of note, the C11orf21 promoter sequence contains a consensus sequence for RUNX1 binding and it was activated by exogenously expressed RUNX1 based on our luciferase reporter assay. This luciferase signal was trans-dominantly suppressed by RUNX1-ETO and site-directed mutagenesis of the consensus site abrogated the reporter activity. This study demonstrated that C11orf21 is a novel transcriptional target of RUNX1 and RUNX1-ETO suppressed C11orf21 transcription in t(8;21) AML. Thus, through this in silico approach, we identified a novel transcriptional target of RUNX1, and the depletion of C11orf21, the target gene, may be associated with the onset of t(8;21) AML.
Keywords	chromosome translocation ; computer simulation ; consensus sequence ; genes ; humans ; luciferase ; myeloid leukemia ; patients ; promoter regions ; site-directed mutagenesis ; transcription (genetics) ; transcription factors
Language	English
Publishing place	Elsevier B.V.
Document type	Article
ISSN	2667-1603
DOI	10.1016/j.bbadva.2022.100047
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