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Article: NF-Y (CBF) regulation in specific cell types and mouse models.

Maity, Sankar N

Biochimica et biophysica acta. Gene regulatory mechanisms

2016 Volume 1860, Issue 5, Page(s) 598–603

Abstract: The CCAAT-binding factor CBF/NF-Y is needed for cell proliferation and early embryonic development. NF-Y can regulate the expression of different cell type-specific genes that are activated by various physiological signaling pathways. Dysregulation of NF- ...

Abstract	The CCAAT-binding factor CBF/NF-Y is needed for cell proliferation and early embryonic development. NF-Y can regulate the expression of different cell type-specific genes that are activated by various physiological signaling pathways. Dysregulation of NF-Y was observed in pathogenic conditions in humans such as scleroderma, neurodegenerative disease, and cancer. Conditional inactivation of the NF-YA gene in mice demonstrated that NF-Y activity is essential for normal tissue homeostasis, survival, and metabolic function. Altogether, NF-Y is an essential transcription factor that plays a critical role in mammalian development, from the early stages to adulthood, and in human pathogenesis. This article is part of a Special Issue entitled: Nuclear Factor Y in Development and Disease, edited by Prof. Roberto Mantovani.
MeSH term(s)	Animals ; CCAAT-Binding Factor/genetics ; CCAAT-Binding Factor/metabolism ; Humans ; Mice ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/metabolism ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Scleroderma, Diffuse/genetics ; Scleroderma, Diffuse/metabolism
Chemical Substances	CCAAT-Binding Factor ; Neoplasm Proteins
Language	English
Publishing date	2016-11-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 1874-9399 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	1874-9399 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439
DOI	10.1016/j.bbagrm.2016.10.014
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Article ; Online: The transcription factor NF-YA is crucial for neural progenitor maintenance during brain development.

Yamanaka, Tomoyuki / Kurosawa, Masaru / Yoshida, Aya / Shimogori, Tomomi / Hiyama, Akiko / Maity, Sankar N / Hattori, Nobutaka / Matsui, Hideaki / Nukina, Nobuyuki

The Journal of biological chemistry

2024 Volume 300, Issue 2, Page(s) 105629

Abstract: In contrast to stage-specific transcription factors, the role of ubiquitous transcription factors in neuronal development remains a matter of scrutiny. Here, we demonstrated that a ubiquitous factor NF-Y is essential for neural progenitor maintenance ... ...

Abstract	In contrast to stage-specific transcription factors, the role of ubiquitous transcription factors in neuronal development remains a matter of scrutiny. Here, we demonstrated that a ubiquitous factor NF-Y is essential for neural progenitor maintenance during brain morphogenesis. Deletion of the NF-YA subunit in neural progenitors by using nestin-cre transgene in mice resulted in significant abnormalities in brain morphology, including a thinner cerebral cortex and loss of striatum during embryogenesis. Detailed analyses revealed a progressive decline in multiple neural progenitors in the cerebral cortex and ganglionic eminences, accompanied by induced apoptotic cell death and reduced cell proliferation. In neural progenitors, the NF-YA short isoform lacking exon 3 is dominant and co-expressed with cell cycle genes. ChIP-seq analysis from the cortex during early corticogenesis revealed preferential binding of NF-Y to the cell cycle genes, some of which were confirmed to be downregulated following NF-YA deletion. Notably, the NF-YA short isoform disappears and is replaced by its long isoform during neuronal differentiation. Forced expression of the NF-YA long isoform in neural progenitors resulted in a significant decline in neuronal count, possibly due to the suppression of cell proliferation. Collectively, we elucidated a critical role of the NF-YA short isoform in maintaining neural progenitors, possibly by regulating cell proliferation and apoptosis. Moreover, we identified an isoform switch in NF-YA within the neuronal lineage in vivo, which may explain the stage-specific role of NF-Y during neuronal development.
MeSH term(s)	Animals ; Mice ; CCAAT-Binding Factor/genetics ; CCAAT-Binding Factor/metabolism ; Cerebral Cortex/cytology ; Cerebral Cortex/growth & development ; Cerebral Cortex/metabolism ; Gene Expression Regulation ; Neurogenesis ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Transcription Factors/metabolism
Chemical Substances	CCAAT-Binding Factor ; Protein Isoforms ; Transcription Factors ; Nfya protein, mouse
Language	English
Publishing date	2024-01-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2024.105629
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Article ; Online: Gene expression profiling in neuronal cells identifies a different type of transcriptome modulated by NF-Y.

Yamanaka, Tomoyuki / Miyazaki, Haruko / Tosaki, Asako / Maity, Sankar N / Shimogori, Tomomi / Hattori, Nobutaka / Nukina, Nobuyuki

Scientific reports

2020 Volume 10, Issue 1, Page(s) 21714

Abstract: A heterotrimeric transcription factor NF-Y is crucial for cell-cycle progression in various types of cells. In contrast, studies using NF-YA knockout mice have unveiled its essential role in endoplasmic reticulum (ER) homeostasis in neuronal cells. ... ...

Abstract	A heterotrimeric transcription factor NF-Y is crucial for cell-cycle progression in various types of cells. In contrast, studies using NF-YA knockout mice have unveiled its essential role in endoplasmic reticulum (ER) homeostasis in neuronal cells. However, whether NF-Y modulates a different transcriptome to mediate distinct cellular functions remains obscure. Here, we knocked down NF-Y in two types of neuronal cells, neuro2a neuroblastoma cells and mouse brain striatal cells, and performed gene expression profiling. We found that down-regulated genes preferentially contained NF-Y-binding motifs in their proximal promoters, and notably enriched genes related to ER functions rather than those for cell cycle. This contrasts with the profiling data of HeLa and embryonic stem cells in which distinct down-regulation of cell cycle-related genes was observed. Clustering analysis further identified several functional clusters where populations of the down-regulated genes were highly distinct. Further analyses using chromatin immunoprecipitation and RNA-seq data revealed that the transcriptomic difference was not correlated with DNA binding of NF-Y but with splicing of NF-YA. These data suggest that neuronal cells have a different type of transcriptome in which ER-related genes are dominantly modulated by NF-Y, and imply that NF-YA splicing alteration could be involved in this cell type-specific gene modulation.
MeSH term(s)	Alternative Splicing ; Animals ; CCAAT-Binding Factor/genetics ; CCAAT-Binding Factor/physiology ; Cell Cycle/genetics ; Endoplasmic Reticulum/genetics ; Gene Expression Profiling ; HeLa Cells ; Homeostasis/genetics ; Humans ; Mice ; Neurons/metabolism ; Neurons/physiology ; RNA Splicing ; Transcriptome/genetics
Chemical Substances	CCAAT-Binding Factor
Language	English
Publishing date	2020-12-10
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/s41598-020-78682-8
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Article: Function of Tumor Suppressors in Resistance to Antiandrogen Therapy and Luminal Epithelial Plasticity of Aggressive Variant Neuroendocrine Prostate Cancers.

Soundararajan, Rama / Aparicio, Ana M / Logothetis, Christopher J / Mani, Sendurai A / Maity, Sankar N

Frontiers in oncology

2018 Volume 8, Page(s) 69

Abstract: Combined loss of tumor suppressors (TSPs), PTEN, TP53, and RB1, is highly associated with small cell carcinoma of prostate phenotype. Recent genomic studies of human tumors as well as analyses in mouse genetic models have revealed a unique role for these ...

Abstract	Combined loss of tumor suppressors (TSPs), PTEN, TP53, and RB1, is highly associated with small cell carcinoma of prostate phenotype. Recent genomic studies of human tumors as well as analyses in mouse genetic models have revealed a unique role for these TSPs in dictating epithelial lineage plasticity-a phenomenon that plays a critical role in the development of aggressive variant prostate cancer (PCa) and associated androgen therapy resistance. Here, we summarize recently published key observations on this topic and hypothesize a possible mechanism by which concurrent loss of TSPs could potentially regulate the PCa disease phenotype.
Language	English
Publishing date	2018-03-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2018.00069
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Article ; Online: Understanding the lethal variant of prostate cancer: power of examining extremes.

Aparicio, Ana / Logothetis, Christopher J / Maity, Sankar N

Cancer discovery

2011 Volume 1, Issue 6, Page(s) 466–468

Abstract: Small cell prostate carcinoma is a lethal variant of castration-resistant prostate cancer. Beltran and colleagues identified overexpression and amplification of both aurora kinase A (AURKA) and the MYCN proto-oncogene in the small cell prostate ... ...

Abstract	Small cell prostate carcinoma is a lethal variant of castration-resistant prostate cancer. Beltran and colleagues identified overexpression and amplification of both aurora kinase A (AURKA) and the MYCN proto-oncogene in the small cell prostate carcinomas and propose Aurora kinase A as a potential therapeutic target in this disease subset.
MeSH term(s)	Antineoplastic Agents/therapeutic use ; Humans ; Male ; Neuroendocrine Tumors/drug therapy ; Neuroendocrine Tumors/genetics ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Protein Kinase Inhibitors/therapeutic use
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors
Language	English
Publishing date	2011-08-25
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-11-0259
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Article ; Online: Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis.

Han, Hyunho / Wang, Yan / Curto, Josue / Gurrapu, Sreeharsha / Laudato, Sara / Rumandla, Alekya / Chakraborty, Goutam / Wang, Xiaobo / Chen, Hong / Jiang, Yan / Kumar, Dhiraj / Caggiano, Emily G / Capogiri, Monica / Zhang, Boyu / Ji, Yan / Maity, Sankar N / Hu, Min / Bai, Shanshan / Aparicio, Ana M /

Efstathiou, Eleni / Logothetis, Christopher J / Navin, Nicholas / Navone, Nora M / Chen, Yu / Giancotti, Filippo G

Cell reports

2022 Volume 39, Issue 1, Page(s) 110595

Abstract: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) ...

Abstract	Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Benzamides ; Carcinoma, Neuroendocrine ; Cell Line, Tumor ; Cell Plasticity/drug effects ; Cell Plasticity/physiology ; Drug Resistance, Neoplasm ; Humans ; Male ; Mice ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Nitriles ; Phenylthiohydantoin ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Receptors, Androgen/drug effects ; Receptors, Androgen/metabolism ; Signal Transduction ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/physiology
Chemical Substances	Antineoplastic Agents ; Benzamides ; Nitriles ; Receptors, Androgen ; Phenylthiohydantoin (2010-15-3) ; enzalutamide (93T0T9GKNU)
Language	English
Publishing date	2022-04-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110595
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Article ; Online: LncRNA-p21 alters the antiandrogen enzalutamide-induced prostate cancer neuroendocrine differentiation via modulating the EZH2/STAT3 signaling.

Luo, Jie / Wang, Keliang / Yeh, Shuyuan / Sun, Yin / Liang, Liang / Xiao, Yao / Xu, Wanhai / Niu, Yuanjie / Cheng, Liang / Maity, Sankar N / Jiang, Runze / Chang, Chawnshang

Nature communications

2019 Volume 10, Issue 1, Page(s) 2571

Abstract: While the antiandrogen enzalutamide (Enz) extends the castration resistant prostate cancer (CRPC) patients' survival an extra 4.8 months, it might also result in some adverse effects via inducing the neuroendocrine differentiation (NED). Here we found ... ...

Abstract	While the antiandrogen enzalutamide (Enz) extends the castration resistant prostate cancer (CRPC) patients' survival an extra 4.8 months, it might also result in some adverse effects via inducing the neuroendocrine differentiation (NED). Here we found that lncRNA-p21 is highly expressed in the NEPC patients derived xenograft tissues (NEPC-PDX). Results from cell lines and human clinical sample surveys also revealed that lncRNA-p21 expression is up-regulated in NEPC and Enz treatment could increase the lncRNA-p21 to induce the NED. Mechanism dissection revealed that Enz could promote the lncRNA-p21 transcription via altering the androgen receptor (AR) binding to different androgen-response-elements, which switch the EZH2 function from histone-methyltransferase to non-histone methyltransferase, consequently methylating the STAT3 to promote the NED. Preclinical studies using the PDX mouse model proved that EZH2 inhibitor could block the Enz-induced NED. Together, these results suggest targeting the Enz/AR/lncRNA-p21/EZH2/STAT3 signaling may help urologists to develop a treatment for better suppression of the human CRPC progression.
MeSH term(s)	Androgen Antagonists/adverse effects ; Animals ; Benzamides ; Cell Differentiation/drug effects ; Cell Differentiation/genetics ; Cell Line, Tumor ; Disease Progression ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Male ; Mice ; Mice, SCID ; Neuroendocrine Cells/drug effects ; Neuroendocrine Cells/pathology ; Neuroendocrine Tumors/drug therapy ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/pathology ; Nitriles ; Phenylthiohydantoin/adverse effects ; Phenylthiohydantoin/analogs & derivatives ; Prostate/cytology ; Prostate/drug effects ; Prostate/pathology ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; RNA, Long Noncoding/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Up-Regulation/drug effects ; Xenograft Model Antitumor Assays
Chemical Substances	Androgen Antagonists ; Benzamides ; Nitriles ; RNA, Long Noncoding ; STAT3 Transcription Factor ; STAT3 protein, human ; Phenylthiohydantoin (2010-15-3) ; enzalutamide (93T0T9GKNU) ; EZH2 protein, human (EC 2.1.1.43) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43)
Language	English
Publishing date	2019-06-12
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/s41467-019-09784-9
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Article ; Online: Inactivation of CBF/NF-Y in postnatal liver causes hepatocellular degeneration, lipid deposition, and endoplasmic reticulum stress.

Luo, Rong / Klumpp, Sherry A / Finegold, Milton J / Maity, Sankar N

Scientific reports

2011 Volume 1, Page(s) 136

Abstract: We previously demonstrated that CBF activity is needed for cell proliferation and early embryonic development. To examine the in vivo function of CBF in differentiated hepatocytes, we conditionally deleted CBF-B in hepatocytes after birth. Deletion of ... ...

Abstract	We previously demonstrated that CBF activity is needed for cell proliferation and early embryonic development. To examine the in vivo function of CBF in differentiated hepatocytes, we conditionally deleted CBF-B in hepatocytes after birth. Deletion of CBF-B resulted in progressive liver injury and severe hepatocellular degeneration 4 weeks after birth. Electron microscopic examination demonstrated pleiotropic changes of hepatocytes including enlarged cell and nuclear size, intracellular lipid deposition, disorganized endoplasmic reticulum, and mitochondrial abnormalities. Gene expression analyses showed that deletion of CBF-B activated expression of specific endoplasmic reticulum (ER) stress-regulated genes. Inactivation of CBF-B also inhibited expression of C/EBP alpha, an important transcription factor controlling various metabolic processes in adult hepatocytes. Altogether, our study reveals for the first time that CBF is a key transcription factor controlling ER function and metabolic processes in mature hepatocytes.
MeSH term(s)	Animals ; Animals, Newborn ; CCAAT-Binding Factor/antagonists & inhibitors ; CCAAT-Binding Factor/deficiency ; CCAAT-Binding Factor/genetics ; Endoplasmic Reticulum Stress ; Fatty Liver/genetics ; Fatty Liver/metabolism ; Fatty Liver/pathology ; Gene Expression ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Hepatomegaly/genetics ; Hepatomegaly/metabolism ; Hepatomegaly/pathology ; Lipid Metabolism ; Liver/injuries ; Liver/metabolism ; Liver/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microscopy, Electron, Transmission
Chemical Substances	CCAAT-Binding Factor
Language	English
Publishing date	2011-11-01
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/srep00136
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Article ; Online: Frequent PTEN loss and differential HER2/PI3K signaling pathway alterations in salivary duct carcinoma: Implications for targeted therapy.

Saintigny, Pierre / Mitani, Yoshitsugu / Pytynia, Kristen B / Ferrarotto, Renata / Roberts, Dianna B / Weber, Randal S / Kies, Merrill S / Maity, Sankar N / Lin, Sue-Hwa / El-Naggar, Adel K

Cancer

2018 Volume 124, Issue 18, Page(s) 3693–3705

Abstract: Background: Patients with advanced primary and recurrent salivary duct carcinoma (SDC), a rare and lethal malignancy, have limited therapeutic options. Novel small-molecule agents aimed at targeting critical signaling associated with SDC tumorigenesis ... ...

Abstract	Background: Patients with advanced primary and recurrent salivary duct carcinoma (SDC), a rare and lethal malignancy, have limited therapeutic options. Novel small-molecule agents aimed at targeting critical signaling associated with SDC tumorigenesis may lead to new therapeutic options for patients with these tumors. The human epidermal growth factor receptor 2 (HER2)/phosphoinositide 3-kinase (PI3K) axis, an important oncogenic pathway, has been targeted for therapy in several solid tumors. Currently, little is known about the role and clinical implications of alterations of the HER2/PI3K pathway in patients with SDC. Methods: The authors investigated the clinicopathologic features, genetic alterations, and expression of key members of the HER2/PI3K pathway in 43 primary tumors and conducted in vitro functional and targeted drug-response analyses on cell lines derived from salivary epithelial carcinomas. Results: In primary tumors, loss of phosphatase and tensin homolog (PTEN) expression was identified in 22 of 43 tumors (51%), overexpression of HER2 was observed in 12 of 43 tumors (28%), and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) mutations were identified in 12 of 43 tumors (28%). Phosphorylated protein kinase B (p-AKT) was highly expressed in most tumors. Most tumors (70%) displayed mutually exclusive alterations of PI3K members, whereas 8 tumors (19%) had 2 or more concurrent abnormalities. In vitro studies demonstrated a direct association between PTEN loss and PI3K pathway activation and evidence of response to combined PI3Kα and PI3Kβ and/or pan-PI3K inhibitors. Conclusions: The current analyses reveal frequent PTEN loss and mutually exclusive alterations of key PI3K pathway members in SDC and demonstrate in vitro evidence of a response to pan-PI3K inhibitors. These results provide a framework for a biomarker-based substratification of patients with SDC in future targeted therapy. Cancer 2018;124:3523-32. © 2018 American Cancer Society.
MeSH term(s)	Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Carcinoma, Ductal/genetics ; Carcinoma, Ductal/therapy ; Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Gene Deletion ; Gene Frequency ; HEK293 Cells ; Humans ; Molecular Targeted Therapy/methods ; Mutation ; PTEN Phosphohydrolase/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, ErbB-2/genetics ; Receptor, ErbB-2/metabolism ; Risk Assessment ; Salivary Gland Neoplasms/genetics ; Salivary Gland Neoplasms/therapy ; Signal Transduction/genetics ; Transcriptome ; Tumor Cells, Cultured
Chemical Substances	Biomarkers, Tumor ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CA protein, human (EC 2.7.1.137) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
Language	English
Publishing date	2018-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1429-1
ISSN	1097-0142 ; 0008-543X ; 1934-662X
ISSN (online)	1097-0142
ISSN	0008-543X ; 1934-662X
DOI	10.1002/cncr.31600
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Article ; Online: CBF/NF-Y controls endoplasmic reticulum stress induced transcription through recruitment of both ATF6(N) and TBP.

Luo, Rong / Lu, Jing-Fang / Hu, Qianghua / Maity, Sankar N

Journal of cellular biochemistry

2008 Volume 104, Issue 5, Page(s) 1708–1723

Abstract: Previously the analysis of promoters regulated by endoplasmic reticulum (ER) stress identified a composite promoter element, ERSE that interacts with both CBF/NF-Y (CBF) and ATF6(N) transcription factors. This prompted us to investigate the underlying ... ...

Abstract	Previously the analysis of promoters regulated by endoplasmic reticulum (ER) stress identified a composite promoter element, ERSE that interacts with both CBF/NF-Y (CBF) and ATF6(N) transcription factors. This prompted us to investigate the underlying mechanism by which CBF, a ubiquitously binding transcription factor, specifically controls transcription activation during ER stress. The in vitro DNA binding study performed using purified recombinant proteins revealed that CBF specifically recruits ATF6(N) to ERSE DNA but it does not interact with ATF6(N) in absence of DNA binding. Inhibition of CBF binding resulted in a significant reduction of optimal transcription activation of cellular genes during ER stress. Analysis of cellular promoters by ChIP demonstrated that CBF is needed for recruitment of both ATF6(N) and TBP but not for either acetylation of histone H3-K9 or trimethylation of histone H3-K4 during ER stress. Together these study results reveal that CBF controls ER stress-inducible transcription through recruitment of both ATF6(N) and TBP but not through chromatin modifications. Our observations are in agreement with the results of recently published studies that have shown that CBF controls transcription of varieties of inducible promoters through recruitment of general transcription factors but not through acetylation of histone H4. These findings provide a paradigm of the function of CBF in inducible transcription.
MeSH term(s)	Activating Transcription Factor 6/metabolism ; Base Sequence ; CCAAT-Binding Factor/metabolism ; Chromatin Immunoprecipitation ; DNA/metabolism ; Endoplasmic Reticulum/pathology ; Gene Expression Regulation, Neoplastic ; HeLa Cells ; Heat-Shock Proteins/genetics ; Humans ; Molecular Chaperones/genetics ; Molecular Sequence Data ; Promoter Regions, Genetic/genetics ; Protein Binding ; RNA, Small Interfering/metabolism ; Recombinant Proteins/isolation & purification ; Recombinant Proteins/metabolism ; TATA-Box Binding Protein/metabolism ; Transcription, Genetic ; Transcriptional Activation/genetics
Chemical Substances	Activating Transcription Factor 6 ; CCAAT-Binding Factor ; Heat-Shock Proteins ; Molecular Chaperones ; RNA, Small Interfering ; Recombinant Proteins ; TATA-Box Binding Protein ; molecular chaperone GRP78 ; DNA (9007-49-2)
Language	English
Publishing date	2008-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.21736
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