Bibliografie tematiche / SREBP

Letteratura scientifica selezionata sul tema "SREBP"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 1 aprile 2023

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Articoli di riviste sul tema "SREBP":

Kober, Daniel L., Shimeng Xu, Shili Li, Bilkish Bajaj, Guosheng Liang, Daniel M. Rosenbaum e Arun Radhakrishnan. "Identification of a degradation signal at the carboxy terminus of SREBP2: A new role for this domain in cholesterol homeostasis". Proceedings of the National Academy of Sciences 117, n. 45 (26 ottobre 2020): 28080–91. http://dx.doi.org/10.1073/pnas.2018578117.

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Lipid homeostasis in animal cells is maintained by sterol regulatory element-binding proteins (SREBPs), membrane-bound transcription factors whose proteolytic activation requires the cholesterol-sensing membrane protein Scap. In endoplasmic reticulum (ER) membranes, the carboxyl-terminal domain (CTD) of SREBPs binds to the CTD of Scap. When cholesterol levels are low, Scap escorts SREBPs from the ER to the Golgi, where the actions of two proteases release the amino-terminal domains of SREBPs that travel to the nucleus to up-regulate expression of lipogenic genes. The CTD of SREBP remains bound to Scap but must be eliminated so that Scap can be recycled to bind and transport additional SREBPs. Here, we provide insights into how this occurs by performing a detailed molecular dissection of the CTD of SREBP2, one of three SREBP isoforms expressed in mammals. We identify a degradation signal comprised of seven noncontiguous amino acids encoded in exon 19 that mediates SREBP2’s proteasomal degradation in the absence of Scap. When bound to the CTD of Scap, this signal is masked and SREBP2 is stabilized. Binding to Scap requires an arginine residue in exon 18 of SREBP2. After SREBP2 is cleaved in Golgi, its CTD remains bound to Scap and returns to the ER with Scap where it is eliminated by proteasomal degradation. The Scap-binding motif, but not the degradation signal, is conserved in SREBP1. SREBP1’s stability is determined by a degradation signal in a different region of its CTD. These findings highlight a previously unknown role for the CTD of SREBPs in regulating SREBP activity.

Zhang, Lijun, Chunyan Li, Fang Wang, Shenghua Zhou, Mingjun Shangguan, Lina Xue, Bianying Zhang et al. "Treatment with PPARαAgonist Clofibrate Inhibits the Transcription and Activation of SREBPs and Reduces Triglyceride and Cholesterol Levels in Liver of Broiler Chickens". PPAR Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/347245.

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PPARαagonist clofibrate reduces cholesterol and fatty acid concentrations in rodent liver by an inhibition of SREBP-dependent gene expression. In present study we investigated the regulation mechanisms of the triglyceride- and cholesterol-lowering effect of the PPARαagonist clofibrate in broiler chickens. We observed that PPARαagonist clofibrate decreases the mRNA and protein levels of LXRαand the mRNA and both precursor and nuclear protein levels of SREBP1 and SREBP2 as well as the mRNA levels of the SREBP1 (FASNandGPAM) and SREBP2 (HMGCRandLDLR) target genes in the liver of treated broiler chickens compared to control group, whereas the mRNA level ofINSIG2, which inhibits SREBP activation, was increased in the liver of treated broiler chickens compared to control group. Taken together, the effects of PPARαagonist clofibrate on lipid metabolism in liver of broiler chickens involve inhibiting transcription and activation of SREBPs and SREBP-dependent lipogenic and cholesterologenic gene expression, thereby resulting in a reduction of the triglyceride and cholesterol levels in liver of broiler chickens.

An, Hyun-Jin, Jung-Yeon Kim, Mi-Gyeong Gwon, Hyemin Gu, Hyun-Ju Kim, Jaechan Leem, Sung Won Youn e Kwan-Kyu Park. "Beneficial Effects of SREBP Decoy Oligodeoxynucleotide in an Animal Model of Hyperlipidemia". International Journal of Molecular Sciences 21, n. 2 (15 gennaio 2020): 552. http://dx.doi.org/10.3390/ijms21020552.

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Hyperlipidemia is a chronic disorder that plays an important role in the development of cardiovascular diseases, type II diabetes, atherosclerosis, hypertension, and non-alcoholic fatty liver disease. Hyperlipidemias have created a worldwide health crisis and impose a substantial burden not only on personal health but also on societies and economies. Transcription factors in the sterol regulatory element binding protein (SREBP) family are key regulators of the lipogenic genes in the liver. SREBPs regulate lipid homeostasis by controlling the expression of a range of enzymes required for the synthesis of endogenous cholesterol, fatty acids, triacylglycerol, and phospholipids. Thereby, SREBPs have been considered as targets for the treatment of metabolic diseases. The aim of this study was to investigate the beneficial functions and the possible underlying molecular mechanisms of SREBP decoy ODN, which is a novel inhibitor of SREBPs, in high-fat diet (HFD)-fed hyperlipidemic mice. Our studies using HFD-induced hyperlipidemia animal model revealed that SREBB decoy ODN inhibited the increased expression of fatty acid synthetic pathway, such as SREBP-1c, FAS, SCD-1, ACC1, and HMGCR. In addition, SREBP decoy ODN decreased pro-inflammatory cytokines, including TNF-α, IL-1β, IL-8, and IL-6 expression. These results suggest that SREBP decoy ODN exerts its anti-hyperlipidemia effects in HFD-induced hyperlipidemia mice by regulating their lipid metabolism and inhibiting lipogenesis through inactivation of the SREPB pathway.

Mahmud, Iqbal, Guimei Tian, Tarun Hutchison, Brandon Kim e Daiqing Liao. "Abstract LB138: DAXX interacts with sterol regulatory element-binding proteins (SREBPs) to promote oncogenic lipogenesis and tumorigenesis in triple-negative breast cancer". Cancer Research 82, n. 12_Supplement (15 giugno 2022): LB138. http://dx.doi.org/10.1158/1538-7445.am2022-lb138.

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Abstract Elevated lipid metabolism including lipogenesis is a major metabolic feature in cancer cells. In breast and other cancer types, genes involved in lipogenesis are highly upregulated, but the mechanisms that control their expression remain poorly understood. DAXX modulates gene expression through binding to numerous transcription factors although the functional impact of these diverse interactions remains to be defined. Our recent analysis indicates that DAXX is overexpressed in diverse cancer types and metastases. However, mechanisms underlying DAXX’s oncogenic function remains elusive. Using global integrated transcriptomic and lipidomic analyses, we show that DAXX plays a key role in lipid metabolism in triple-negative breast cancer (TNBC) cells. DAXX depletion attenuates, while its overexpression enhances, lipogenic gene expression, lipid synthesis and tumor growth. Mechanistically, DAXX interacts with SREBP1 and SREBP2 and activates SREBP-mediated transcription. DAXX associates with lipogenic gene promoters through SREBPs. Underscoring the critical roles for the DAXX-SREBP interaction for lipogenesis, SREBP2 knockdown attenuates tumor growth in cells with DAXX overexpression, and a DAXX mutant unable to bind SREBPs are incapable of promoting lipogenesis and tumor growth. In TNBC patients, DAXX expression levels are increased in breast cancer brain metastasis and correlate with poor patient survival. Our results identify the DAXX-SREBP axis as an important pathway for tumorigenesis in TNBC. (This work is supported by Florida Department of Health Grants.) Citation Format: Iqbal Mahmud, Guimei Tian, Tarun Hutchison, Brandon Kim, Daiqing Liao. DAXX interacts with sterol regulatory element-binding proteins (SREBPs) to promote oncogenic lipogenesis and tumorigenesis in triple-negative breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr LB138.

Wang, Hang, Feng Liu, Clarke F. Millette e Daniel L. Kilpatrick. "Expression of a Novel, Sterol-Insensitive Form of Sterol Regulatory Element Binding Protein 2 (SREBP2) in Male Germ Cells Suggests Important Cell- and Stage-Specific Functions for SREBP Targets during Spermatogenesis". Molecular and Cellular Biology 22, n. 24 (15 dicembre 2002): 8478–90. http://dx.doi.org/10.1128/mcb.22.24.8478-8490.2002.

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ABSTRACT Cholesterol biosynthesis in somatic cells is controlled at the transcriptional level by a homeostatic feedback pathway involving sterol regulatory element binding proteins (SREBPs). These basic helix-loop-helix (bHLH)-Zip proteins are synthesized as membrane-bound precursors, which are cleaved to form a soluble, transcriptionally active mature SREBP that regulates the promoters for genes involved in lipid synthesis. Homeostasis is conferred by sterol feedback inhibition of this maturation process. Previous work has demonstrated the expression of SREBP target genes in the male germ line, several of which are highly up-regulated during specific developmental stages. However, the role of SREBPs in the control of sterol regulatory element-containing promoters during spermatogenesis has been unclear. In particular, expression of several of these genes in male germ cells appears to be insensitive to sterols, contrary to SREBP-dependent gene regulation in somatic cells. Here, we have characterized a novel isoform of the transcription factor SREBP2, which is highly enriched in rat and mouse spermatogenic cells. This protein, SREBP2gc, is expressed in a stage-dependent fashion as a soluble, constitutively active transcription factor that is not subject to feedback control by sterols. These findings likely explain the apparent sterol-insensitive expression of lipid synthesis genes during spermatogenesis. Expression of a sterol-independent, constitutively active SREBP2gc in the male germ line may have arisen as a means to regulate SREBP target genes in specific developmental stages. This may reflect unique roles for cholesterol synthesis and other functional targets of SREBPs during spermatogenesis.

Bien, Clara M., e Peter J. Espenshade. "Sterol Regulatory Element Binding Proteins in Fungi: Hypoxic Transcription Factors Linked to Pathogenesis". Eukaryotic Cell 9, n. 3 (29 gennaio 2010): 352–59. http://dx.doi.org/10.1128/ec.00358-09.

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ABSTRACT Sterol regulatory element binding proteins (SREBPs) are membrane-bound transcription factors whose proteolytic activation is controlled by the cellular sterol concentration. Mammalian SREBPs are activated in cholesterol-depleted cells and serve to regulate cellular lipid homeostasis. Recent work demonstrates that SREBP is functionally conserved in fungi. While the ability to respond to sterols is conserved, fungal SREBPs are hypoxic transcription factors required for adaptation to a low-oxygen environment. In the fission yeast Schizosaccharomyces pombe, oxygen regulates the SREBP homolog Sre1 by independently controlling both its proteolytic activation and its degradation. SREBP is also required for adaptation to hypoxia in the human pathogens Cryptococcus neoformans and Aspergillus fumigatus. In these organisms, SREBP is required for virulence and resistance to antifungal drugs, making the SREBP pathway a potential target for antifungal therapy.

RIDGWAY, Neale D., e Thomas A. LAGACE. "Regulation of the CDP-choline pathway by sterol regulatory element binding proteins involves transcriptional and post-transcriptional mechanisms". Biochemical Journal 372, n. 3 (15 giugno 2003): 811–19. http://dx.doi.org/10.1042/bj20030252.

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The synthesis of phosphatidylcholine (PtdCho) by the CDP-choline pathway is under the control of the rate-limiting enzyme CTP:phosphocholine cytidylyltransferase (CCT). Sterol regulatory element binding proteins (SREBPs) have been proposed to regulate CCT at the transcriptional level, or via the synthesis of lipid activators or substrates of the CDP-choline pathway. To assess the contributions of these two mechanisms, we examined CCTα expression and PtdCho synthesis by the CDP-choline pathway in cholesterol and fatty acid auxotrophic CHO M19 cells inducibly expressing constitutively active nuclear forms of SREBP1a or SREBP2. Induction of either SREBP resulted in increased expression of mRNAs for sterol-regulated genes, elevated fatty acid and cholesterol synthesis (>10–50-fold) and increased PtdCho synthesis (2-fold). CCTα mRNA was increased 2-fold by enforced expression of SREBP1a or SREBP2. The resultant increase in CCTα protein and activity (2-fold) was restricted primarily to the soluble fraction of cells, and increased CCTα activity in vivo was not detected. Inhibition of the synthesis of fatty acids or their CoA esters by cerulenin or triacsin C respectively following SREBP induction effectively blocked the accompanying elevation in PtdCho synthesis. Thus PtdCho synthesis was driven by increased synthesis of fatty acids or a product thereof. These data show that transcriptional activation of CCTα is modest relative to that of other SREBP-regulated genes, and that stimulation of PtdCho synthesis by SREBPs in CHO cells is due primarily to increased fatty acid synthesis.

Zoumi, Aikaterini, Shrimati Datta, Lih-Huei L. Liaw, Cristen J. Wu, Gopi Manthripragada, Timothy F. Osborne e Vickie J. LaMorte. "Spatial Distribution and Function of Sterol Regulatory Element-Binding Protein 1a and 2 Homo- and Heterodimers by In Vivo Two-Photon Imaging and Spectroscopy Fluorescence Resonance Energy Transfer". Molecular and Cellular Biology 25, n. 8 (15 aprile 2005): 2946–56. http://dx.doi.org/10.1128/mcb.25.8.2946-2956.2005.

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ABSTRACT Sterol regulatory element-binding proteins (SREBPs) are a subfamily of basic helix-loop-helix-leucine zipper proteins that regulate lipid metabolism. We show novel evidence of the in vivo occurrence and subnuclear spatial localization of both exogenously expressed SREBP-1a and -2 homodimers and heterodimers obtained by two-photon imaging and spectroscopy fluorescence resonance energy transfer. SREBP-1a homodimers localize diffusely in the nucleus, whereas SREBP-2 homodimers and the SREBP-1a/SREBP-2 heterodimer localize predominantly to nuclear speckles or foci, with some cells showing a diffuse pattern. We also used tethered SREBP dimers to demonstrate that both homo- and heterodimeric SREBPs activate transcription in vivo. Ultrastructural analysis revealed that the punctate foci containing SREBP-2 are electron-dense nuclear bodies, similar or identical to structures containing the promyelocyte (PML) protein. Immunofluorescence studies suggest that a dynamic interplay exists between PML, as well as another component of the PML-containing nuclear body, SUMO-1, and SREBP-2 within these nuclear structures. These findings provide new insight into the overall process of transcriptional activation mediated by the SREBP family.

Amemiya-Kudo, Michiyo, Hitoshi Shimano, Alyssa H. Hasty, Naoya Yahagi, Tomohiro Yoshikawa, Takashi Matsuzaka, Hiroaki Okazaki et al. "Transcriptional activities of nuclear SREBP-1a, -1c, and -2 to different target promoters of lipogenic and cholesterogenic genes". Journal of Lipid Research 43, n. 8 (agosto 2002): 1220–35. http://dx.doi.org/10.1194/jlr.m100417-jlr200.

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Recent studies on the in vivo roles of the sterol regulatory element binding protein (SREBP) family indicate that SREBP-2 is more specific to cholesterogenic gene expression whereas SREBP-1 targets lipogenic genes. To define the molecular mechanism involved in this differential regulation, luciferase-reporter gene assays were performed in HepG2 cells to compare the transactivities of nuclear SREBP-1a, -1c, and -2 on a battery of SREBP-target promoters containing sterol regulatory element (SRE), SRE-like, or E-box sequences. The results show first that cholesterogenic genes containing classic SREs in their promoters are strongly and efficiently activated by both SREBP-1a and SREBP-2, but not by SREBP-1c. Second, an E-box containing reporter gene is much less efficiently activated by SREBP-1a and -1c, and SREBP-2 was inactive in spite of its ability to bind to the E-box. Third, promoters of lipogenic enzymes containing variations of SRE (SRE-like sequences) are strongly activated by SREBP-1a, and only modestly and equally by both SREBP-1c and -2. Finally, substitution of the unique tyrosine residue within the basic helix-loop-helix (bHLH) portion of nuclear SREBPs with arginine, the conserved residue found in all other bHLH proteins, abolishes the transactivity of all SREBPs for SRE, and conversely results in markedly increased activity of SREBP-1 but not activity of SREBP-2 for E-boxes.These data demonstrate the different specificity and affinity of nuclear SREBP-1 and -2 for different target DNAs, explaining a part of the mechanism behind the differential in vivo regulation of cholesterogenic and lipogenic enzymes by SREBP-1 and -2, respectively.

Inoue, Noriyuki, Hitoshi Shimano, Masanori Nakakuki, Takashi Matsuzaka, Yoshimi Nakagawa, Takashi Yamamoto, Ryuichiro Sato et al. "Lipid Synthetic Transcription Factor SREBP-1a Activates p21WAF1/CIP1, a Universal Cyclin-Dependent Kinase Inhibitor". Molecular and Cellular Biology 25, n. 20 (15 ottobre 2005): 8938–47. http://dx.doi.org/10.1128/mcb.25.20.8938-8947.2005.

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ABSTRACT Sterol regulatory element-binding proteins (SREBPs) are membrane-bound transcription factors that regulate lipid synthetic genes. In contrast to SREBP-2, which regulates cellular cholesterol level in normal cells, SREBP-1a is highly expressed in actively growing cells and activates entire programs of genes involved in lipid synthesis such as cholesterol, fatty acids, triglycerides, and phospholipids. Previously, the physiological relevance of this potent activity of SREBP-1a has been thought to regulate the supply of membrane lipids in response to cell growth. Here we show that nuclear SREBP-1a and SREBP-2 bind directly to a novel SREBP binding site in the promoter of the p21WAF1/CIP1 gene, the major cyclin-dependent kinase inhibitor, and strongly activate its promoter activity. Only the SREBP-1a isoform consistently causes induction of p21 at both the mRNA and protein levels. Colony formation assays and polyploidy of livers from transgenic mice suggest that activation of p21 by SREBP-1a could inhibit cell growth. Activation of endogenous SREBPs in lipid deprivation conditions was associated with induction of p21 mRNA and protein. Expression of p21 was reduced in SREBP-1 null mice. These data suggest a physiological role of SREBP-1a in p21 regulation. Identification of p21 as a new SREBP target might implicate a new paradigm in the link between lipid synthesis and cell growth.

Più fonti

Tesi sul tema "SREBP":

Wu, Jiakai. "Primary rat hepatocyte isolation and culture regulates the SREBP/SREBP target gene profile". Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491482.

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The major limitation of using primary hepatocytes is the rapid dedifferentiation of hepatocytes during isolation and culture, whereby most of the liver-specific functions are lost. Despite the many efforts that have been made to optimize the culture condition, current primary cultured hepatocyte preparations still only retain partial hepatocyte phenotype observed in liver in vivo. To further optimize primary hepatocytes it is essential to understand the key factors that underlie the dedifferentiation process during primary hepatocyte culture. Up or down-regulation of key transcription factors has been observed during primary hepatocyte culture, which could lead to dramatic change of downstream target genes. In my study, the influence of primary hepatocyte culture on the expression of a more ubiquitously expressed transcription factor family called sterol regulatory element binding protein (SREBP) was examined. SREBP transcriptionally regulates genes involved in glucose metabolism, lipognesis and cholesterolgenesis, which are the three important functions of liver. I compared the expression of SREBP and putative SREBP target genes in two culture media- one of which was a basic support for primary hepatocyte culture (MM) and the second of which was . designed to sustain hepatocytes in a more differentiated state for a prolonged period (HepatozymeÃ‚Â™). I showed that mRNA encoding SREBP and putative SREBP target genes decreased during culture in MM, but that HepatozymeÃ‚Â™ selectively improved mRNA expression for SREBP-2 and NF-Y and all the putative SREBP target genes which contain SRE/NF-Y composite elements in their promoters (FAS, 514, HMGCR and squalene synthase). Genes that lacked the SRE/NF-Y structure within their promoters (SREBP-1a, GK, L-PK and PEPCK) showed a decreased mRNA profile during culture in both medium conditions. Transcription factors involved in the transcriptional activation of GK, PEPCK and SREBP-1a (including LXR-a, HNF-4a and Sp1) also exhibited a decreased profile during culture in both medium conditions. My data indicates that improved expression of specific transcription factors during primary hepatocyte culture could underlie the recovery of a subset of downstream target genes. However, the number of improved transcription factors was small, which suggests that further improvement of the expression of transcription factors would be an important aspect for the maintenance of primary hepatocyte gene expression. My studies have provided an approach of understanding the relationship between the status of key transcription factors with that of downstream target genes during primary hepatocyte culture, and this could be a good starting point of understanding a broader aspect of key transcription factors that is involved in the maintenance of global gene expression during primary hepatocyte culture.

Le, Lay Soazig. "Rôle des facteurs de transcription SREBP dans le métabolisme adipocytaire : implication de SREBP-1c dans la réponse à l'insuline et activation de SREBP-2 au cours de l'obésité". Paris 6, 2003. http://www.theses.fr/2003PA066188.

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Iddon, Christopher R. "Investigation of the putative sterol pool that regulates SREBP cleavage". Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392930.

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Yecies, Jessica. "SREBP: A Key Effector of mTORC1 Signaling in Metabolism and Cancer". Thesis, Harvard University, 2011. http://dissertations.umi.com/gsas.harvard:10023.

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The mammalian target of rapamycin complex 1 (mTORC1), a master regulator of cell growth and proliferation, is aberrantly activated in cancer, genetic tumor syndromes and obesity. Much progress has been made to understand the upstream pathways that regulate mTORC1, most of which converge upon its negative regulator, the Tuberous Sclerosis Complex (TSC) 1-TSC2 complex. However, the cell intrinsic consequences of aberrant mTORC1 activation remain poorly characterized. Using systems in which mTORC1 is constitutively activated by genetic loss of TSC1 or TSC2 and pharmacologically inhibited by treatment with an mTORC1-specific inhibitor rapamycin, we have identified that mTORC1 controls specific aspects of cellular metabolism, including glycolysis, the pentose phosphate pathway, and de novo lipogenesis. Induction of the pentose phosphate pathway and de novo lipogenesis is achieved by activation of a transcriptional program affecting metabolic gene targets of sterol regulatory element-binding protein (SREBP). We have demonstrated that mTORC1 stimulates the accumulation of processed, active SREBP, although details of the molecular mechanism remain to be elucidated. To understand the physiological and pathological relevance of mTORC1-dependent activation of SREBPs and lipogenesis, we explored these findings in the liver and in cancer. While we find that the induction of hepatic SREBP1c and lipogenesis by insulin requires mTORC1, mTORC1 activation is not sufficient to stimulate hepatic SREBP1c in the absence of Akt signaling, revealing the existence of an additional downstream pathway also required for this induction. We demonstrate that this mTORC1-independent pathway involves Akt-mediated suppression of Insig2a, a liver-specific transcript encoding the SREBP1c inhibitor INSIG2. In cancer, our initial findings demonstrate that mTORC1 plays a role downstream of TSC-deficiency and oncogenic PIK3CA and K-Ras to activate lipogenic SREBP targets and de novo lipogenesis. Further studies of the connection between mTORC1 and SREBPs in disease may offer insights into novel therapeutic approaches.

Ricoult, Stephane Jean Hermann. "Oncogenic Control and Metabolic Outputs of the Lipogenic Transcription Factor SREBP". Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493542.

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The sterol regulatory element binding protein (SREBP) transcription factors have emerged as central regulators of de novo lipogenesis in the liver. However, while it is known that lipid synthesis is elevated in many cancers, much less is known about the control of lipid metabolism in this context. The goals of this dissertation were to better understand the mechanisms through which commonly mutated oncogenes and tumor suppressors promote de novo lipid synthesis, and to further define the importance of this process in cancer. Using isogenic oncogene-expressing breast epithelial cells and breast cancer cell lines, I have identified a major mechanism through which two of the most commonly activated oncogenes in cancer promote de novo lipogenesis. In particular, I found that the expression of oncogenic PI3K or K-Ras is sufficient to stimulate de novo lipid synthesis in breast epithelial cells through the activation of mechanistic target of rapamycin complex 1 (mTORC1) and SREBP. Consistent with these findings, increased mTORC1 signaling in breast cancer patient tumor samples is associated with elevated expression of canonical SREBP targets involved in de novo lipogenesis. I further demonstrate that SREBP depletion in breast cancer cells or in oncogene-expressing epithelial cells reduces growth-factor independent proliferation. To better understand the role of SREBP in cancer metabolism, I sought to determine whether SREBP regulates isocitrate dehydrogenase 1 (IDH1), which is both a metabolic enzyme and an oncogene. Specifically, I show that SREBP activates the expression of IDH1 across a panel of cancer cell lines from different lineages, and that IDH1 expression facilitates the flux of glutamine-derived carbons towards de novo lipid synthesis. In addition, SREBP stimulates the expression of oncogenic IDH1R132C, which is a neomorphic enzyme that produces the oncometabolite 2-hydroxyglutarate, and can regulate 2-hydroxyglutarate production in mutant-IDH1 cells. Collectively, these studies expand our understanding of lipid metabolism in cancer and identify important roles for SREBP in cancer cell metabolism and proliferation. Our results will help guide future studies on the regulation of SREBP, the role of SREBP targets, and the production of specific lipid species in cancer, which will hopefully identify novel therapeutic targets to treat cancer patients.
Medical Sciences

Eid, Walaa. "mTORC1 Activates SREBP-2 through Maintenance of Endosomal Cycling and Suppression of Autophagy". Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/36473.

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The mammalian target of rapamycin complex 1 (mTORC1) is known to regulate lipogenesis through sterol regulatory element binding proteins (SREBPs), master regulators of cholesterol and fatty acid synthesis. Through an incompletely understood mechanism, mTORC1 triggers translocation of SREBPs, an endoplasmic reticulum (ER) resident protein, to the Golgi, where mature SREBP is proteolytically produced to activate transcription of lipogenic genes. Low ER cholesterol is a well-known trigger for SREBPs activation, which includes translocation, maturation, and transcriptional activation. The study investigated whether mTORC1 activates SREBP by limiting cholesterol delivery to the ER. The findings indicate an increase in mTORC1 activity is accompanied by lower ER cholesterol and by SREBP-2 activation, a transcription factor primarily responsible for cholesterol synthesis. A decrease in mTORC1 activity, on another hand, coincides with higher ER cholesterol and lower SERBP-2 activity. I further report that this ER cholesterol is of lysosomal origin, as blocking the exit of cholesterol from lysosomes by U18666A or NPC1 siRNA prevents ER cholesterol from rising and, consequently, SREBP-2 is activated without mTORC1 activation. I identified two membrane trafficking processes, triggered by low mTORC1 activity, supply the lysosomes with cholesterol: autophagy and re-routing of endosomes to lysosomes. Indeed, a dual blockade by Atg5-/- and rab5 kept the ER cholesterol low even when mTORC1 activity was low, and resulted in SREBP-2 activation. Conversely, over-expressing Atg7, which forces autophagy, raises the ER cholesterol and suppresses SREBP-2 activity even when mTORC1 activity is high. Thus, it can be concluded that mTORC1 actively suppresses the formation of autophagosomes and promotes endosomal recycling, both of which prevents cholesterol to reach the lysosomes, thereby reducing cholesterol levels in the ER and activating SREBP-2.

Dif, Nicolas. "Expression et régulation du facteur de transcription SREBP-1c humain : rôle de l'insuline". Lyon 1, 2006. http://www.theses.fr/2006LYO10216.

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SREBP-1c belongs to a family of transcription factors (SREBPs : Sterol Regulatory Element Binding Proteins) originally found to be involved in the cholesterol and fatty acid metabolism and in adipocyte differentiation. SREBP-1c has been implicated in the effect of insulin and nutritional environment on gene expression. Therefore, study of insulin action on SREBP-1c is important to enhance knowledge of mechanisms involved in insulin action and in type 2 diabetes. During my PhD, I first study the role of SREBP-1c on carbohydrates and lipid metabolism, in focus on key genes of theses metabolic pathways, during nutritional changes. Next, I characterized the human SREBP-1c promoter and determined a region responsible for the insulin action on this promoter. I demonstrated that the mechanisms implies are differents between human and rodents and that trancriptional action of insulin essentially involves SREBP-1c itself
SREBP-1c est un facteur de transcription de la famille SREBP (Sterol Regulatory Element Binding Protein. Plusieurs groupes ont mis en évidence le rôle de la protéine SREBP-1c dans la régulation de l’expression génique en réponse à l’insuline et aux variations nutritionnelles. L’étude de la régulation de SREBP-1c par l’insuline devrait donc nous permettre de mieux appréhender les mécanismes d'action de l'insuline. Au cours de ma thèse, j’ai tout d’abord étudié le rôle joué par le facteur SREBP-1c dans les principaux tissus insulino-sensibles sur le contrôle du métabolisme glucidique et lipidique, en étudiant la régulation de gènes clés de ces voies métaboliques, lors de variations de l'état nutritionnel. Ensuite, j’ai caractérisé le promoteur humain de SREBP-1c et déterminé les régions responsables de l’action de l’insuline. J’ai montré que les mécanismes impliqués étaient différents de ceux observés chez les rongeurs et que l’action transcriptionnelle de l’insuline implique essentiellement le facteur SREBP-1c lui-même

Liang, Wentao. "Myostatin promotes liver fat accumulation through activation of the mTOR-SREBP-1c pathway". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12479.

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Abstract (sommario):

Thesis (M.A.)--Boston University
Myostatin is a cytokine primarily expressed in skeletal muscle and heart muscle and acts as a negative regulator for muscle development. Inhibition of myostatin by genetic and pharmacological approaches improves metabolic health, which has been generally considered as secondary to the hypermuscularity and insulin hyper-sensitivity. Although the receptor for myostatin is ubiquitously expressed, whether and how myostatin interacts with other metabolically important cell types remain largely unknown. In this work, we provide multiple lines of evidence that myostatin directly interacts with hepatocytes. Furthermore, we show for the first time that myostatin enhances insulin signaling in both cultured hepatocytes and in mouse liver. Mice injected with adena-associated virus encoding myostatin propeptide, an endogenous myostatin inhibitor, were partially protected from diet-induced liver fat accumulation and reduced lipogenic gene expression. Consistent with the in vivo findings, increased lipid accumulation was found in cells treated with myostatin peptide or transfected with myostatin construct. Myostatin promotes the lipogenic effect of insulin by enhancing nuclear translocation of SREBP-1c, the master lipogenic transcription factor and increases expression of its downstream target genes. This effect was found to be associated with myostatin-related mTOR activation. Blocking mTOR activation by rapamycin prevents myostatinassociated increase of nuclear SREBP-1 c and its downstream lipogenic enzymes. In summary, this work identified liver as a direct target of myostatin, providing the first evidence that myostatin has opposite impacts on insulin signaling in muscle cells and hepatocytes. Our data also provided a novel mechanism for the long-term metabolic protection afforded by anti-myostatin treatments demonstrated in this work as well as elsewhere.

Ma, Liying. "Regulatory factors of milk fat synthesis in dairy cows". Diss., Virginia Tech, 2012. http://hdl.handle.net/10919/29120.

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The objective of these studies was to investigate the milk fat synthesis regulation by transcription factors. In the first study, bovine mammary epithelial (MAC-T) cells were treated with sterol regulatory element binding protein-1 (SREBP-1) specific siRNA. The mRNA and protein expression of SREBP-1 were decreased by more than 90% by siRNA. Fatty acid (FA) synthesis, uptake, and selected lipogenic enzyme expression were reduced in cells treated with SREBP-1 siRNA. Therefore, SREBP-1 plays an important role in integrated regulation of lipid synthesis in MAC-T cells through regulation of key enzymes. In the second study, MAC-T cells treated with hormones or FA were transfected with luciferase reporter constructs containing response elements for SREBP-1, peroxisome proliferator-activated receptor Î³ (PPARÎ³), or liver X receptor (LXR). The activation of PPARÎ³ and SREBP-1 were stimulated by insulin and insulin combined with leptin, respectively. Trans-10, cis-12 conjugated linoleic acid (CLA) inhibited SREBP-1 activation, and this inhibition was not attenuated by insulin and leptin. Neither trans-10 nor cis-12 double bond inhibited SREBP-1 activation. Taken together, trans-10 and cis-12 double bonds need to be conjugated in CLA to reduce SREBP-1 activation and this inhibition cannot be overcome by insulin and leptin combination in MAC-T cells. In the third study, lactating dairy cows were intravenously infused with 0.625 g/h trans-10, cis-12 CLA for 14 h. We confirmed the appearance of trans-10, cis-12 CLA in the milk of CLA treated cows. Milk and component yield were not affected by the CLA treatment. The desaturation of stearic acid was reduced by CLA. The mRNA and protein expression of transcription factors or lipogenic enzymes were not affected by trans-10, cis-12 CLA. DNA-binding activities for PPARÎ³ and LXR and the activation of SREBP-1 to its mature form were not changed by the treatment. The infusion time in this study was probably too short to induce any changes in transcription factors and lipogenic enzymes. We confirmed DNA-binding activities of PPARÎ³ and LXR in bovine mammary gland. Overall, a prominent role for SREBP-1 in mammary epithelial cell lipid synthetic pathways was described and regulation of transcription factor activation by trans-10, cis-12 CLA was specific to SREBP-1.
Ph. D.

Asano, Lisa. "Vitamin D metabolite, 25-Hydroxyvitamin D, regulates lipid metabolism by inducing degradation of SREBP/SCAP". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225512.

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Libri sul tema "SREBP":

Misbahuddin. Statin Pharmacogenetics in Metabolic Syndrome- The SREBP-SCAP Pathway. Germany: LAP LAMBERT Academic Publishing, 2012.

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Southern Regional Education Board. Commission for Educational Quality, a cura di. A Progress report and recommendations on educational improvements in the SREB states: A report to the Southern Regional Education Board. Atlanta, Ga: SREB, 1987.

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Gaines, Gale F. Educational Goals in Sreb States. Southern Regional Education Board, 1990.

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Marks, Joseph L. Sreb Fact Book on Higher Education (Sreb Fact Book on Higher Education 1998 99). Southern Regional Education Board, 1999.

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Marks, Joseph L. Sreb Fact Book on Higher Education 2000/2001 (Sreb Fact Book on Higher Education). Southern Regional Education Board, 2001.

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Marks, Joseph L. Sreb Fact Book on Higher Education. Southern Regional Education Board, 1995.

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Sreb Fact Book on Higher Education, 1990. Southern Regional Educ Board, 1990.

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Marks, Joseph L. Sreb Fact Book on Higher Education, 1990. Southern Regional Education Board, 1990.

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Marks, Joseph Lappin. Sreb Fact Book on Higher Education, 1992. Southern Regional Education Board, 1993.

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Crews, Alton Dr. Making Leadership Happen: The Sreb Model for Leadership. Southern Regional Education Board, 1996.

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Capitoli di libri sul tema "SREBP":

Ishida, Chiaki T., Wei Shao e Peter J. Espenshade. "Assaying Sterol-Regulated ER-to-Golgi Transport of SREBP Cleavage-Activating Protein Using Immunofluorescence Microscopy". In Methods in Molecular Biology, 755–64. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2639-9_45.

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Inoue, Jun, e Ryuichiro Sato. "Transcriptional Regulation of the Genes for Human HMG CoA Synthase and Squalene Synthase by SREBP and NF-Y". In Lipoprotein Metabolism and Atherogenesis, 149–51. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_32.

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Shimano, Hitoshi, e Nobuhiro Yamada. "In vivo Functions of SREBPs". In Lipoprotein Metabolism and Atherogenesis, 137–41. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_28.

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Wolberg, Hans-Bernd. "SREP – Neues Prüfungskonzept der Bankenaufsicht". In Complexity Kills - Banken im Dickicht von Regulierung und verkrusteten Strukturen, 53–67. Wiesbaden: Springer Fachmedien Wiesbaden, 2020. http://dx.doi.org/10.1007/978-3-658-29287-4_5.

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Bai, Yongxiu, e Songji Wang. "Framework of the SREB Initiative". In Spirit of the Silk Road, 1–42. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4541-9_1.

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Bai, Yongxiu, e Songji Wang. "Guarantee Mechanism for the SREB". In Spirit of the Silk Road, 217–67. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4541-9_7.

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Barton, Larry L., e Guy D. Fauque. "Systems Contributing to the Energetics of SRBP". In Sulfate-Reducing Bacteria and Archaea, 245–93. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-96703-1_5.

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Boudra, Safia, Itheri Yahiaoui e Ali Behloul. "Statistical Radial Binary Patterns (SRBP) for Bark Texture Identification". In Advanced Concepts for Intelligent Vision Systems, 101–13. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-70353-4_9.

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Speth, Michael. "Der neue SREP-Ansatz der internationalen Bankenaufsicht: Fortschritt oder Rückschritt?" In Die neue Welt der Banken, 33–51. Wiesbaden: Springer Fachmedien Wiesbaden, 2016. http://dx.doi.org/10.1007/978-3-658-14822-5_3.

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Kotzka, Jörg, Wilhelm Krone e Dirk Müller-Wieland. "Sterol-regulatory element binding proteins (SREBPs): gene-regulatory target of statin action". In HMG-CoA Reductase Inhibitors, 35–54. Basel: Birkhäuser Basel, 2002. http://dx.doi.org/10.1007/978-3-0348-8135-7_3.

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Atti di convegni sul tema "SREBP":

Ramachandran, Vimal, e S. Hani Najafi-shoushtari. "Srebp-2 Intronic Microrna 33a Post-translationally Controls Ldl Uptake". In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2014. http://dx.doi.org/10.5339/qfarc.2014.hbpp1091.

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plantier, laurent, Valérie Besnard e Jeffrey Whitsett. "Insig1 Regulates SREBP Mediated Lipogenesis In Alveolar Type 2 Cells". In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4953.

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cheng, chunming, feng geng, xiang cheng, arnab chakravarti e deliang guo. "Abstract 1457: SCAP/SREBP-1 regulates lipid metabolism reprogramming in cancer cell". In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1457.

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Han, Chun-Chun, Ji-Wen Wang, Liang Li e Wei Wang. "The cDNA Segment Cloning and Bioinformatics Analysis of SREBP-2 Gene in Goose". In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE 2009). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5163582.

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LaMorte, Vickie J., Aikaterini Zoumi, Shrimati Datta, Cristen J. Wu e Timothy Osborne. "Utilization of two-photon FRET to monitor SREBP homodimer and heterodimer formation in living cells". In Biomedical Optics 2003, a cura di Ammasi Periasamy e Peter T. C. So. SPIE, 2003. http://dx.doi.org/10.1117/12.478034.

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Li, Xiangyan, Yi-Ting Chen, Leland W. K. Chung e Wen-Chin Huang. "Abstract 4728: Fatostatin, a novel SREBP inhibitor, suppresses cell growth and induces apoptosis in prostate cancer". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4728.

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Torres-Ayuso, PEDRO, David Jones, Maria Tello-Lafoz, Antonia Avila-Flores e Isabel Merida. "Abstract 35: Diacylglycerol kinase zeta-mediated regulation of mTOR and SREBP-1 offers new opportunities for cancer management". In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-35.

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Wang, Li, Chun-Chun Han, Ji-Wen Wang, Liang Li e Zhong-Xian Zhang. "Effect of Exogenous Cholesterol on Cholesterol Accumulation and mRNA Expression of SREBP-2 and HMGR in Goose Primary Hepatocytes". In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE 2009). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5162694.

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Zhang, Xiaoxia, Yuan He, Yan Chen, Airong Zhang, Jing Sun e Tian Li. "Regulation of FFA metabolism and attenuation of lipid accumulation through AMPK/SREBP-1c signaling by the extract of Apium graveolens L. root". In ICBET 2022: 2022 12th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3535694.3535719.

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Guan, Min. "Abstract 2653: Nelfinavir induces apoptosis in hormone-resistant prostate cancer cells through inhibition of regulated intramembrane proteolysis of SREBP-1 and ATF6". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2653.

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Rapporti di organizzazioni sul tema "SREBP":

Moore, Gary. 1997 Summer Research Program (SRP), Summer Research Extension Program (SREP), Final Report, Volume 3. Rome Laboratory. Fort Belvoir, VA: Defense Technical Information Center, dicembre 1997. http://dx.doi.org/10.21236/ada386997.

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Moore, Gary. 1997 Summer Research Program (SRP), Summer Research Extension Program (SREP), Final Report, Volume 2. Phillips Laboratory. Fort Belvoir, VA: Defense Technical Information Center, dicembre 1997. http://dx.doi.org/10.21236/ada387081.

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Moore, Gary. 1997 Summer Research Program (SRP), Summer Research Extension Program (SREP), Final Report, Volume 1. Program Management and Armstrong Laboratory. Fort Belvoir, VA: Defense Technical Information Center, dicembre 1997. http://dx.doi.org/10.21236/ada387080.

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Moore, Gary. 1997 Summer Research Program (SRP), Summer Research Extension Program (SREP), Final Report, Volume 5. Arnold Engineering Center, Air Logistics Centers, United States Air Force Academy, Wilford Hall Medical Center. Fort Belvoir, VA: Defense Technical Information Center, dicembre 1997. http://dx.doi.org/10.21236/ada387014.

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