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Article ; Online: An Updated View of the Roles of p53 in Embryonic Stem Cells.

Ayaz, Gamze / Yan, Hualong / Malik, Navdeep / Huang, Jing

2022 Volume 40, Issue 10, Page(s) 883–891

Abstract: The TP53 gene is unarguably one of the most studied human genes. Its encoded protein, p53, is a tumor suppressor and is often called the "guardian of the genome" due to its pivotal role in maintaining genome stability. Historically, most studies of p53 ... ...

Abstract	The TP53 gene is unarguably one of the most studied human genes. Its encoded protein, p53, is a tumor suppressor and is often called the "guardian of the genome" due to its pivotal role in maintaining genome stability. Historically, most studies of p53 have focused on its roles in somatic cells and tissues, but in the last 2 decades, its functions in embryonic stem cells (ESCs) and induced pluripotent stem cells have attracted increasing attention. Recent studies have identified p53 as a critical regulator of pluripotency, self-renewal, differentiation, proliferation, and genome stability in mouse and human embryonic stem cells. In this article, we systematically review the studies on the functions of p53 in ESCs, provide an updated overview, attempt to reconcile controversial results described in the literature, and discuss the relevance of these cellular functions of p53 to its roles in tumor suppression.
MeSH term(s)	Animals ; Humans ; Mice ; Cell Differentiation/genetics ; Embryonic Stem Cells/metabolism ; Genes, p53 ; Genomic Instability ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53 ; TP53 protein, human
Language	English
Publishing date	2022-07-28
Publishing country	England
Document type	Systematic Review ; Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1093/stmcls/sxac051
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Article ; Online: Autophagy Inhibition as a Potential Therapeutic Strategy for Breast Cancer with Mitochondrial Translation Defect Caused by CBFB-Deficiency.

Malik, Navdeep / Yan, Hualong / Kim, Young-Im / Ayaz, Gamze / Wang, Shasha / Mondal, Payel / Luo, Ji / Huang, Jing

Autophagy

2023 Volume 19, Issue 11, Page(s) 3026–3028

Abstract: Abbreviations: AMPK, AMP-activated protein kinase; BioID, biotinylation identification; CBFB, core-binding factor subunit beta; HCQ, hydroxychloroquine; HNRNPK, heterogeneous nuclear ribonucleoprotein K; PDX, patient-derived xenograft; PIK3CA, ... ...

Abstract	Abbreviations: AMPK, AMP-activated protein kinase; BioID, biotinylation identification; CBFB, core-binding factor subunit beta; HCQ, hydroxychloroquine; HNRNPK, heterogeneous nuclear ribonucleoprotein K; PDX, patient-derived xenograft; PIK3CA, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; TUFM, Tu translation elongation factor, mitochondrial; ETC, electron transport chain.
MeSH term(s)	Humans ; Female ; Autophagy ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Mitochondria/metabolism ; Core Binding Factor beta Subunit/metabolism
Chemical Substances	CBFB protein, human ; Core Binding Factor beta Subunit
Language	English
Publishing date	2023-05-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Comment
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2023.2208481
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Article: SOX9 is a key component of RUNX2-regulated transcriptional circuitry in osteosarcoma.

Kim, Young-Im / Tseng, Yu-Chou / Ayaz, Gamze / Wang, Shasha / Yan, Hualong / du Bois, Wendy / Yang, Howard / Zhen, Tao / Lee, Maxwell P / Liu, Paul / Kaplan, Rosandra N / Huang, Jing

Cell & bioscience

2023 Volume 13, Issue 1, Page(s) 136

Abstract: Background: The absence of prominent, actionable genetic alternations in osteosarcomas (OS) implies that transcriptional and epigenetic mechanisms significantly contribute to the progression of this life-threatening form of cancer. Therefore, the ... ...

Abstract	Background: The absence of prominent, actionable genetic alternations in osteosarcomas (OS) implies that transcriptional and epigenetic mechanisms significantly contribute to the progression of this life-threatening form of cancer. Therefore, the identification of potential transcriptional events that promote the survival of OS cells could be key in devising targeted therapeutic approaches for OS. We have previously shown that RUNX2 is a transcription factor (TF) essential for OS cell survival. Unfortunately, the transcriptional network or circuitry regulated by RUNX2 in OS cells is still largely unknown. Methods: The TFs that are in the RUNX2 transcriptional circuitry were identified by analyzing RNAseq and ChIPseq datasets of RUNX2. To evaluate the effect of SOX9 knockdown on the survival of osteosarcoma cells in vitro, we employed cleaved caspase-3 immunoblotting and propidium iodide staining techniques. The impact of SOX9 and JMJD1C depletion on OS tumor growth was examined in vivo using xenografts and immunohistochemistry. Downstream targets of SOX9 were identified and dissected using RNAseq, pathway analysis, and gene set enrichment analysis. Furthermore, the interactome of SOX9 was identified using BioID and validated by PLA. Result: Our findings demonstrate that SOX9 is a critical TF that is induced by RUNX2. Both in vitro and in vivo experiments revealed that SOX9 plays a pivotal role in the survival of OS. RNAseq analysis revealed that SOX9 activates the transcription of MYC, a downstream target of RUNX2. Mechanistically, our results suggest a transcriptional network involving SOX9, RUNX2, and MYC, with SOX9 binding to RUNX2. Moreover, we discovered that JMJD1C, a chromatin factor, is a novel binding partner of SOX9, and depletion of JMJD1C impairs OS tumor growth. Conclusion: The findings of this study represent a significant advancement in our understanding of the transcriptional network present in OS cells, providing valuable insights that may contribute to the development of targeted therapies for OS.
Language	English
Publishing date	2023-07-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2593367-X
ISSN	2045-3701
ISSN	2045-3701
DOI	10.1186/s13578-023-01088-2
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Article ; Online: Estradiol-Estrogen Receptor α Mediates the Expression of the CXXC5 Gene through the Estrogen Response Element-Dependent Signaling Pathway.

Yaşar, Pelin / Ayaz, Gamze / Muyan, Mesut

Scientific reports

2016 Volume 6, Page(s) 37808

Abstract: 17β-estradiol (E2), the primary circulating estrogen hormone, mediates physiological and pathophysiological functions of breast tissue mainly through estrogen receptor α (ERα). Upon binding to E2, ERα modulates the expression of target genes involved in ... ...

Abstract	17β-estradiol (E2), the primary circulating estrogen hormone, mediates physiological and pathophysiological functions of breast tissue mainly through estrogen receptor α (ERα). Upon binding to E2, ERα modulates the expression of target genes involved in the regulation of cellular proliferation primarily through interactions with specific DNA sequences, estrogen response elements (EREs). Our previous microarray results suggested that E2-ERα modulates CXXC5 expression. Because of the presence of a zinc-finger CXXC domain (ZF-CXXC), CXXC5 is considered to be a member of the ZF-CXXC family, which binds to non-methylated CpG dinucleotides. Although studies are limited, CXXC5 appears to participate as a transcription factor, co-regulator and/or epigenetic factor in the regulation of cellular events induced by various signaling pathways. However, how signaling pathways mediate the expression of CXXC5 is yet unclear. Due to the importance of E2-ERα signaling in breast tissue, changes in the CXXC5 transcription/synthesis could participate in E2-mediated cellular events as well. To address these issues, we initially examined the mechanism whereby E2-ERα regulates CXXC5 expression. We show here that CXXC5 is an E2-ERα responsive gene regulated by the interaction of E2-ERα with an ERE present at a region upstream of the initial translation codon of the gene.
MeSH term(s)	Carrier Proteins/genetics ; Cell Line ; Estradiol/metabolism ; Estrogen Receptor alpha/metabolism ; Humans ; Signal Transduction
Chemical Substances	CXXC5 protein, human ; Carrier Proteins ; Estrogen Receptor alpha ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2016--25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep37808
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Article ; Online: Dysregulation of Mitochondrial Translation Caused by CBFB Deficiency Cooperates with Mutant PIK3CA and Is a Vulnerability in Breast Cancer.

Malik, Navdeep / Kim, Young-Im / Yan, Hualong / Tseng, Yu-Chou / du Bois, Wendy / Ayaz, Gamze / Tran, Andy D / Vera-Ramirez, Laura / Yang, Howard / Michalowski, Aleksandra M / Kruhlak, Michael / Lee, Maxwell / Hunter, Kent W / Huang, Jing

Cancer research

2023 Volume 83, Issue 8, Page(s) 1280–1298

Abstract: Understanding functional interactions between cancer mutations is an attractive strategy for discovering unappreciated cancer pathways and developing new combination therapies to improve personalized treatment. However, distinguishing driver gene pairs ... ...

Abstract	Understanding functional interactions between cancer mutations is an attractive strategy for discovering unappreciated cancer pathways and developing new combination therapies to improve personalized treatment. However, distinguishing driver gene pairs from passenger pairs remains challenging. Here, we designed an integrated omics approach to identify driver gene pairs by leveraging genetic interaction analyses of top mutated breast cancer genes and the proteomics interactome data of their encoded proteins. This approach identified that PIK3CA oncogenic gain-of-function (GOF) and CBFB loss-of-function (LOF) mutations cooperate to promote breast tumor progression in both mice and humans. The transcription factor CBFB localized to mitochondria and moonlighted in translating the mitochondrial genome. Mechanistically, CBFB enhanced the binding of mitochondrial mRNAs to TUFM, a mitochondrial translation elongation factor. Independent of mutant PI3K, mitochondrial translation defects caused by CBFB LOF led to multiple metabolic reprogramming events, including defective oxidative phosphorylation, the Warburg effect, and autophagy/mitophagy addiction. Furthermore, autophagy and PI3K inhibitors synergistically killed breast cancer cells and impaired the growth of breast tumors, including patient-derived xenografts carrying CBFB LOF and PIK3CA GOF mutations. Thus, our study offers mechanistic insights into the functional interaction between mutant PI3K and mitochondrial translation dysregulation in breast cancer progression and provides a strong preclinical rationale for combining autophagy and PI3K inhibitors in precision medicine for breast cancer. Significance: CBFB-regulated mitochondrial translation is a regulatory step in breast cancer metabolism and synergizes with mutant PI3K in breast cancer progression.
MeSH term(s)	Animals ; Female ; Humans ; Mice ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Core Binding Factor beta Subunit/genetics ; Core Binding Factor beta Subunit/pharmacology ; Mutation ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors/pharmacology ; Signal Transduction/genetics
Chemical Substances	CBFB protein, human ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Core Binding Factor beta Subunit ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Phosphoinositide-3 Kinase Inhibitors ; PIK3CA protein, human (EC 2.7.1.137)
Language	English
Publishing date	2023-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-2525
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Article ; Online: Author Correction: CXXC5 as an unmethylated CpG dinucleotide binding protein contributes to estrogen-mediated cellular proliferation.

Ayaz, Gamze / Razizadeh, Negin / Yaşar, Pelin / Kars, Gizem / Kahraman, Deniz Cansen / Saatci, Özge / Şahin, Özgür / Çetin-Atalay, Rengül / Muyan, Mesut

Scientific reports

2020 Volume 10, Issue 1, Page(s) 9943

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper. ...

Abstract	An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Language	English
Publishing date	2020-06-16
Publishing country	England
Document type	Published Erratum
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-66682-7
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Article ; Online: CXXC5 as an unmethylated CpG dinucleotide binding protein contributes to estrogen-mediated cellular proliferation.

Ayaz, Gamze / Razizadeh, Negin / Yaşar, Pelin / Kars, Gizem / Kahraman, Deniz Cansen / Saatci, Özge / Şahin, Özgür / Çetin-Atalay, Rengül / Muyan, Mesut

Scientific reports

2020 Volume 10, Issue 1, Page(s) 5971

Abstract: Evidence suggests that the CXXC type zinc finger (ZF-CXXC) protein 5 (CXXC5) is a critical regulator/integrator of various signaling pathways that include the estrogen (E2)-estrogen receptor α (ERα). Due to its ZF-CXXC domain, CXXC5 is considered to be a ...

Abstract	Evidence suggests that the CXXC type zinc finger (ZF-CXXC) protein 5 (CXXC5) is a critical regulator/integrator of various signaling pathways that include the estrogen (E2)-estrogen receptor α (ERα). Due to its ZF-CXXC domain, CXXC5 is considered to be a member of the ZF-CXXC family, which binds to unmethylated CpG dinucleotides of DNA and through enzymatic activities for DNA methylation and/or chromatin modifications generates a chromatin state critical for gene expressions. Structural/functional features of CXXC5 remain largely unknown. CXXC5, suggested as transcription and/or epigenetic factor, participates in cellular proliferation, differentiation, and death. To explore the role of CXXC5 in E2-ERα mediated cellular events, we verified by generating a recombinant protein that CXXC5 is indeed an unmethylated CpG binder. We uncovered that CXXC5, although lacks a transcription activation/repression function, participates in E2-driven cellular proliferation by modulating the expression of distinct and mutual genes also regulated by E2. Furthermore, we found that the overexpression of CXXC5, which correlates with mRNA and protein levels of ERα, associates with poor prognosis in ER-positive breast cancer patients. Thus, CXXC5 as an unmethylated CpG binder contributes to E2-mediated gene expressions that result in the regulation of cellular proliferation and may contribute to ER-positive breast cancer progression.
MeSH term(s)	Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/physiology ; DNA-Binding Proteins/metabolism ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Signal Transduction/drug effects ; Transcription Factors/metabolism
Chemical Substances	CXXC5 protein, human ; DNA-Binding Proteins ; Estrogen Receptor alpha ; Transcription Factors ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2020-04-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-62912-0
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Article ; Online: Dynamic transcriptional events mediated by estrogen receptor alpha.

Ayaz, Gamze / Yasar, Pelin / Olgun, Cagla Ece / Karakaya, Burcu / Kars, Gizem / Razizadeh, Negin / Yavuz, Kerim / Turan, Gizem / Muyan, Mesut

Frontiers in bioscience (Landmark edition)

2019 Volume 24, Issue 2, Page(s) 245–276

Abstract: 17beta-estradiol (E2), the main circulating estrogen hormone, is involved in a wide variety of physiological functions ranging from the development to the maintenance of many tissues and organs. The effects of E2 on cells are primarily conveyed by the ... ...

Abstract	17beta-estradiol (E2), the main circulating estrogen hormone, is involved in a wide variety of physiological functions ranging from the development to the maintenance of many tissues and organs. The effects of E2 on cells are primarily conveyed by the transcription factors, estrogen receptor (ER) alpha and beta. The regulation of responsive genes by the well-defined ER alpha in response to E2 relies on complex and highly organized processes that dynamically integrate functions of many transcription regulators to induce spatiotemporal alterations in chromatin state and structure. Changes in gene expressions result in cell-specific responses that include proliferation, differentiation and death. Deregulation of E2-ER alpha signaling contributes to the initiation and progression of target tissue malignancies. We aim here to provide a review of recent findings on dynamic transcriptional events mediated by E2-ER alpha with the anticipation that a better understanding of complex regulatory mechanisms underlying ER actions would be a critical basis for the development of effective prognostic tools for and therapeutic interventions against estrogen target tissue malignancies.
MeSH term(s)	Animals ; Binding Sites/genetics ; Estradiol/blood ; Estradiol/pharmacology ; Estrogen Receptor alpha/chemistry ; Estrogen Receptor alpha/metabolism ; Humans ; Models, Molecular ; Nucleic Acid Conformation ; Protein Domains ; Response Elements/genetics ; Transcription, Genetic/drug effects
Chemical Substances	Estrogen Receptor alpha ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2019-01-01
Publishing country	Singapore
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2704569-9
ISSN	2768-6698 ; 1093-9946
ISSN (online)	2768-6698
ISSN	1093-9946
DOI	10.2741/4716
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Article ; Online: A CpG island promoter drives the CXXC5 gene expression.

Yaşar, Pelin / Kars, Gizem / Yavuz, Kerim / Ayaz, Gamze / Oğuztüzün, Çerağ / Bilgen, Ecenaz / Suvacı, Zeynep / Çetinkol, Özgül Persil / Can, Tolga / Muyan, Mesut

Scientific reports

2021 Volume 11, Issue 1, Page(s) 15655

Abstract: CXXC5 is a member of the zinc-finger CXXC family that binds to unmethylated CpG dinucleotides. CXXC5 modulates gene expressions resulting in diverse cellular events mediated by distinct signaling pathways. However, the mechanism responsible for CXXC5 ... ...

Abstract	CXXC5 is a member of the zinc-finger CXXC family that binds to unmethylated CpG dinucleotides. CXXC5 modulates gene expressions resulting in diverse cellular events mediated by distinct signaling pathways. However, the mechanism responsible for CXXC5 expression remains largely unknown. We found here that of the 14 annotated CXXC5 transcripts with distinct 5' untranslated regions encoding the same protein, transcript variant 2 with the highest expression level among variants represents the main transcript in cell models. The DNA segment in and at the immediate 5'-sequences of the first exon of variant 2 contains a core promoter within which multiple transcription start sites are present. Residing in a region with high G-C nucleotide content and CpG repeats, the core promoter is unmethylated, deficient in nucleosomes, and associated with active RNA polymerase-II. These findings suggest that a CpG island promoter drives CXXC5 expression. Promoter pull-down revealed the association of various transcription factors (TFs) and transcription co-regulatory proteins, as well as proteins involved in histone/chromatin, DNA, and RNA processing with the core promoter. Of the TFs, we verified that ELF1 and MAZ contribute to CXXC5 expression. Moreover, the first exon of variant 2 may contain a G-quadruplex forming region that could modulate CXXC5 expression.
MeSH term(s)	CpG Islands ; DNA Methylation ; DNA-Binding Proteins ; Histones/metabolism ; Signal Transduction ; Transcription Factors ; Zinc Fingers
Chemical Substances	CXXC5 protein, human ; DNA-Binding Proteins ; Histones ; Transcription Factors
Language	English
Publishing date	2021-08-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-95165-6
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Article ; Online: A prelude to the proximity interaction mapping of CXXC5.

Ayaz, Gamze / Turan, Gizem / Olgun, Çağla Ece / Kars, Gizem / Karakaya, Burcu / Yavuz, Kerim / Demiralay, Öykü Deniz / Can, Tolga / Muyan, Mesut / Yaşar, Pelin

Scientific reports

2021 Volume 11, Issue 1, Page(s) 17587

Abstract: CXXC5 is a member of the zinc-finger CXXC family proteins that interact with unmodified CpG dinucleotides through a conserved ZF-CXXC domain. CXXC5 is involved in the modulation of gene expressions that lead to alterations in diverse cellular events. ... ...

Abstract	CXXC5 is a member of the zinc-finger CXXC family proteins that interact with unmodified CpG dinucleotides through a conserved ZF-CXXC domain. CXXC5 is involved in the modulation of gene expressions that lead to alterations in diverse cellular events. However, the underlying mechanism of CXXC5-modulated gene expressions remains unclear. Proteins perform their functions in a network of proteins whose identities and amounts change spatiotemporally in response to various stimuli in a lineage-specific manner. Since CXXC5 lacks an intrinsic transcription regulatory function or enzymatic activity but is a DNA binder, CXXC5 by interacting with proteins could act as a scaffold to establish a chromatin state restrictive or permissive for transcription. To initially address this, we utilized the proximity-dependent biotinylation approach. Proximity interaction partners of CXXC5 include DNA and chromatin modifiers, transcription factors/co-regulators, and RNA processors. Of these, CXXC5 through its CXXC domain interacted with EMD, MAZ, and MeCP2. Furthermore, an interplay between CXXC5 and MeCP2 was critical for a subset of CXXC5 target gene expressions. It appears that CXXC5 may act as a nucleation factor in modulating gene expressions. Providing a prelude for CXXC5 actions, our results could also contribute to a better understanding of CXXC5-mediated cellular processes in physiology and pathophysiology.
MeSH term(s)	Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Female ; Humans ; MCF-7 Cells ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Methyl-CpG-Binding Protein 2/genetics ; Methyl-CpG-Binding Protein 2/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Protein Interaction Domains and Motifs ; Signal Transduction ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	CXXC5 protein, human ; DNA-Binding Proteins ; MECP2 protein, human ; Membrane Proteins ; Methyl-CpG-Binding Protein 2 ; Nuclear Proteins ; Transcription Factors ; c-MYC-associated zinc finger protein ; emerin
Language	English
Publishing date	2021-09-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-97060-6
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