Publications
53 results found
Rial SA, You Z, Vivoli A, et al., 2024, 14-3-3ζ regulates adipogenesis by modulating chromatin accessibility during the early stages of adipocyte differentiation., bioRxiv
We previously established the scaffold protein 14-3-3ζ as a critical regulator of adipogenesis and adiposity, but the temporal specificity of its action during adipocyte differentiation remains unclear. To decipher if 14-3-3ζ exerts its regulatory functions on mature adipocytes or on adipose precursor cells (APCs), we generated Adipoq14-3-3ζKO and Pdgfra14-3-3ζKO mouse models. Our findings revealed a pivotal role for 14-3-3ζ in APC differentiation in a sex-dependent manner, whereby male and female Pdgfra14-3-3ζKO mice display impaired or potentiated weight gain, respectively, as well as fat mass. To better understand how 14-3-3ζ regulates the adipogenic transcriptional program in APCs, CRISPR-Cas9 was used to generate TAP-tagged 14-3-3ζ-expressing 3T3-L1 preadipocytes. Using these cells, we examined if the 14-3-3ζ nuclear interactome is enriched with adipogenic regulators during differentiation. Regulators of chromatin remodeling, such as DNMT1 and HDAC1, were enriched in the nuclear interactome of 14-3-3ζ, and their activities were impacted upon 14-3-3ζ depletion. The interactions between 14-3-3ζ and chromatin-modifying enzymes suggested that 14-3-3ζ may control chromatin remodeling during adipogenesis, and this was confirmed by ATAC-seq, which revealed that 14-3-3ζ depletion impacted the accessibility of up to 1,244 chromatin regions corresponding in part to adipogenic genes, promoters, and enhancers during the initial stages of adipogenesis. Moreover, 14-3-3ζ-dependent chromatin accessibility was found to directly correlate with the expression of key adipogenic genes. Altogether, our study establishes 14-3-3ζ as a crucial epigenetic regulator of adipogenesis and highlights the usefulness of deciphering the nuclear 14-3-3ζ interactome to identify novel pro-adipogenic factors and pathways.
Chabosseau P, Yong F, Delgadillo-Silva LF, et al., 2023, Molecular phenotyping of single pancreatic islet leader beta cells by "Flash-Seq", Life Sciences, Vol: 316, ISSN: 0024-3205
AIMS: Spatially-organized increases in cytosolic Ca2+ within pancreatic beta cells in the pancreatic islet underlie the stimulation of insulin secretion by high glucose. Recent data have revealed the existence of subpopulations of beta cells including "leaders" which initiate Ca2+ waves. Whether leader cells possess unique molecular features, or localisation, is unknown. MAIN METHODS: High speed confocal Ca2+ imaging was used to identify leader cells and connectivity analysis, running under MATLAB and Python, to identify highly connected "hub" cells. To explore transcriptomic differences between beta cell sub-groups, individual leaders or followers were labelled by photo-activation of the cryptic fluorescent protein PA-mCherry and subjected to single cell RNA sequencing ("Flash-Seq"). KEY FINDINGS: Distinct Ca2+ wave types were identified in individual islets, with leader cells present in 73 % (28 of 38 islets imaged). Scale-free, power law-adherent behaviour was also observed in 29 % of islets, though "hub" cells in these islets did not overlap with leaders. Transcripts differentially expressed (295; padj < 0.05) between leader and follower cells included genes involved in cilium biogenesis and transcriptional regulation. Providing some support for these findings, ADCY6 immunoreactivity tended to be higher in leader than follower cells, whereas cilia number and length tended to be lower in the former. Finally, leader cells were located significantly closer to delta, but not alpha, cells in Euclidian space than were follower cells. SIGNIFICANCE: The existence of both a discrete transcriptome and unique localisation implies a role for these features in defining the specialized function of leaders. These data also raise the possibility that localised signalling between delta and leader cells contributes to the initiation and propagation of islet Ca2+ waves.
Chabosseau P, Yong F, Delgadillo-Silva LF, et al., 2022, Molecular phenotyping of single pancreatic islet leader beta cells by “Flash-Seq”
<jats:title>Abstract</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>Spatially-organised increases in cytosolic Ca<jats:sup>2+</jats:sup>within pancreatic beta cells in the pancreatic islet underlie the stimulation of insulin secretion by high glucose. Recent data have revealed the existence of subpopulations of beta cells including “leaders” which initiate Ca<jats:sup>2+</jats:sup>waves. Whether leader cells possess unique molecular features, or localisation, is unknown.</jats:p></jats:sec><jats:sec><jats:title>Main methods</jats:title><jats:p>High speed confocal Ca<jats:sup>2+</jats:sup>imaging was used to identify leader cells and connectivity analysis, running under MATLAB and Python, to identify highly connected “hub” cells. To explore transcriptomic differences between beta cell sub-groups, individual leaders or followers were labelled by photo-activation of the cryptic fluorescent protein PA-mCherry and subjected to single cell RNA sequencing (“Flash-Seq”).</jats:p></jats:sec><jats:sec><jats:title>Key findings</jats:title><jats:p>Distinct Ca<jats:sup>2+</jats:sup>wave types were identified in individual islets, with leader cells present in 73 % (28 of 38 islets imaged). Scale-free, power law-adherent behaviour was also observed in 29% of islets, though “hub” cells in these islets did not overlap with leaders. Transcripts differentially expressed (295; padj<0.05) between leader and follower cells included genes involved in cilium biogenesis and transcriptional regulation. Functionally validating these findings, cilia number and length tended to be lower in leader<jats:italic>vs</jats:italic>follower cells. Leader cells were also located significantly closer to delta cells in Euclidian space than were follower cells.</jats:p>
Cheung R, Pizza G, Chabosseau P, et al., 2022, Glucose-Dependent miR-125b Is a Negative Regulator of β-Cell Function, DIABETES, Vol: 71, Pages: 1525-1545, ISSN: 0012-1797
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- Citations: 4
Chabosseau PL, Yong SWF, Lopez L, et al., 2022, A Transcriptomic Signature of Pancreatic Islet Leader Beta Cells, Publisher: AMER DIABETES ASSOC, ISSN: 0012-1797
Rial SA, Alkhoury A, Lavoie G, et al., 2022, Critical Cellular Functions That Mediate the Early Stages of Adipogenesis Are Directly Influenced by 14-3-3zeta and Its Interactome, Publisher: AMER DIABETES ASSOC, ISSN: 0012-1797
Nguyen-Tu M-S, Harris J, Martinez-Sanchez A, et al., 2022, Opposing effects on regulated insulin secretion of acute vs chronic stimulation of AMP-activated protein kinase, DIABETOLOGIA, Vol: 65, Pages: 997-1011, ISSN: 0012-186X
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- Citations: 3
Georgia S, Arda HE, Martinez-Sanchez A, et al., 2022, Editorial: Epigenetics of Glucose Homeostasis, FRONTIERS IN ENDOCRINOLOGY, Vol: 13, ISSN: 1664-2392
Salowka A, Martinez-Sanchez A, 2021, Molecular Mechanisms of Nutrient-Mediated Regulation of MicroRNAs in Pancreatic β-cells, FRONTIERS IN ENDOCRINOLOGY, Vol: 12, ISSN: 1664-2392
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- Citations: 2
Martinez-Sanchez A, Cheung R, Pizza G, et al., 2021, Beta cell miR-125b controls glucose homeostasis by targeting lysosomal and mitochondrial genes, Publisher: SPRINGER, Pages: 158-158, ISSN: 0012-186X
Cheung R, Pizza G, Chabosseau P, et al., 2021, Glucose-dependent miR-125b is a negative regulator of β-cell function, BioRxiv
<jats:title>SUMMARY</jats:title><jats:p>Impaired pancreatic β-cell function and insulin secretion are hallmarks of type 2 diabetes. MicroRNAs are short non-coding RNAs that silence gene expression, vital for the development and function of β-cells. MiR-125b-5p (miR-125b), a highly conserved miRNA, is abundant in β-cells, though its role in these cells is unclear. Here we show that miR-125b levels in human islets correlate with body mass index (BMI), and its expression is regulated by glucose in an AMP-activated protein kinase-dependent manner. An unbiased high-throughput screen identified multiple miR-125b targets, including the transporter of lysosomal hydrolases <jats:italic>M6pr</jats:italic> and the mitochondrial fission regulator <jats:italic>Mtfp1</jats:italic>. Inactivation of miR-125b in human β-cells shortened mitochondria and enhanced glucose-stimulated insulin secretion, whilst mice over-expressing miR-125b selectively in β-cells were glucose intolerant. β-cells from these animals contained enlarged lysosomal structures and showed reduced insulin content and secretion. Thus, we identify miR125b as a glucose-controlled regulator of organelle dynamics that modulates insulin secretion.</jats:p><jats:sec id="s1"><jats:title>Highlights</jats:title><jats:list list-type="bullet"><jats:list-item><jats:p>Islet miR-125b correlates with BMI and is regulated by glucose via AMP-activated protein kinase in β-cells</jats:p></jats:list-item><jats:list-item><jats:p>miR-125b targets dozens of genes including several involved in the regulation of mitochondrial (<jats:italic>Mtfp1</jats:italic>) and lysosomal (<jats:italic>M6pr</jats:italic>) morphology or function</jats:p></jats:list-item><jats:list-item><jats:p>Deletion of miR-125b results in shorter mitochondria an
Chabosseau PL, Martinez-Sanchez A, Leclerc I, et al., 2021, Repetitive Ca2+Waves Emanate from a Stable Leader Cell in Mouse Islets, 81st Virtual Scientific Sessions of the American-Diabetes-Association (ADA), Publisher: AMER DIABETES ASSOC, ISSN: 0012-1797
Cheung R, Pizza G, Chabosseau P, et al., 2021, miR-125b impairs beta cell function <i>in vivo</i> by targeting lysosomal and mitochondrial genes, Publisher: WILEY, ISSN: 0742-3071
Mousavy Gharavy SN, Owen BM, Millership SJ, et al., 2021, Sexually dimorphic roles for the type 2 diabetes-associated C2cd4b gene in murine glucose homeostasis, Diabetologia, Vol: 64, Pages: 850-864, ISSN: 0012-186X
Aims/hypothesisVariants close to the VPS13C/C2CD4A/C2CD4B locus are associated with altered risk of type 2 diabetes in genome-wide association studies. While previous functional work has suggested roles for VPS13C and C2CD4A in disease development, none has explored the role of C2CD4B.MethodsCRISPR/Cas9-induced global C2cd4b-knockout mice and zebrafish larvae with c2cd4a deletion were used to study the role of this gene in glucose homeostasis. C2 calcium dependent domain containing protein (C2CD)4A and C2CD4B constructs tagged with FLAG or green fluorescent protein were generated to investigate subcellular dynamics using confocal or near-field microscopy and to identify interacting partners by mass spectrometry.ResultsSystemic inactivation of C2cd4b in mice led to marked, but highly sexually dimorphic changes in body weight and glucose homeostasis. Female C2cd4b mice displayed unchanged body weight compared with control littermates, but abnormal glucose tolerance (AUC, p = 0.01) and defective in vivo, but not in vitro, insulin secretion (p = 0.02). This was associated with a marked decrease in follicle-stimulating hormone levels as compared with wild-type (WT) littermates (p = 0.003). In sharp contrast, male C2cd4b null mice displayed essentially normal glucose tolerance but an increase in body weight (p < 0.001) and fasting blood glucose (p = 0.003) after maintenance on a high-fat and -sucrose diet vs WT littermates. No metabolic disturbances were observed after global inactivation of C2cd4a in mice, or in pancreatic beta cell function at larval stages in C2cd4a null zebrafish. Fasting blood glucose levels were also unaltered in adult C2cd4a-null fish. C2CD4B and C2CD4A were partially localised to the plasma membrane, with the latter under the control of intracellular Ca2+. Binding partners for both included secretory-granule-localised PTPRN2/phogrin.Conclusions/interpretationOur studies sugge
Nguyen-Tu M-S, Martinez-Sanchez A, Leclerc I, et al., 2021, Adipocyte-specific deletion of <i>Tcf7l2</i> induces dysregulated lipid metabolism and impairs glucose tolerance in mice, DIABETOLOGIA, Vol: 64, Pages: 129-141, ISSN: 0012-186X
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- Citations: 12
Rutter GA, Georgiadou E, Martinez-Sanchez A, et al., 2020, Metabolic and functional specialisations of the pancreatic beta cell: gene disallowance, mitochondrial metabolism and intercellular connectivity, DIABETOLOGIA, Vol: 63, Pages: 1990-1998, ISSN: 0012-186X
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- Citations: 43
Lopez-Noriega L, Callingham R, Martinez-Sánchez A, et al., 2020, Roles for the long non-coding RNA<i>Pax6os1</i>/<i>PAX6-AS1</i>in pancreatic beta cell identity and function
<jats:title>Abstract</jats:title><jats:sec><jats:title>Aim/Hypothesis</jats:title><jats:p>Long non-coding RNAs (lncRNAs) are emerging as crucial regulators of beta cell development and function. Here, we investigate roles for an antisense lncRNA expressed from the<jats:italic>Pax6</jats:italic>locus (annotated as<jats:italic>Pax6os1</jats:italic>in mice and<jats:italic>PAX6-AS1</jats:italic>in humans) in beta cell identity and functionality.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p><jats:italic>Pax6os1</jats:italic>expression was silenced in MIN6 cells using siRNAs and changes in gene expression were determined by RNA sequencing or qRT-PCR. Mice inactivated for<jats:italic>Pax6os1</jats:italic>and human<jats:italic>PAX6-AS1</jats:italic>-null EndoC-βH1 cells, were generated using CRISPR/Cas9 technology. Human islets were infected with lentiviral vectors bearing a targeted shRNA or<jats:italic>PAX6-AS1</jats:italic>, which were used to silence or overexpress, respectively, the lncRNA. RNA sequencing or RT-qPCR were used to measure transcriptomic changes and RNA pulldown in mice and human cells followed by mass spectrometry/western blot were performed to explore RNA protein interactions.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>Pax6os1/PAX6-AS1</jats:italic>expression was upregulated at high glucose concentrations in derived beta cell lines as well as in mouse and human islets, and in pancreatic islets isolated from mice fed a high fat diet (n=6, p=0.003) and patients with type 2 diabetes (n=11-5, p<0.01). Silencing or deletion of<jats:italic>Pax6os1</jats:italic>/<jats:italic>PAX6-AS1</jats:italic>in MIN6 or EndoC-βH1cells increased the expression of several
Nguyen-Tu M-S, Martinez-Sanchez A, Leclerc I, et al., 2020, Reduced expression of TCF7L2 in adipocyte impairs glucose tolerance associated with decreased insulin secretion, incretins levels and lipid metabolism dysregulation in male mice
<jats:title>Abstract</jats:title><jats:p>Transcription factor 7-like 2 (TCF7L2) is a downstream effector of the Wnt/beta-catenin signalling pathway and its expression is critical for adipocyte development. The precise role of TCF7L2 in glucose and lipid metabolism in adult adipocytes remains to be defined. Here, we aim to investigate how changes in TCF7L2 expression in mature adipocytes affect glucose homeostasis. <jats:italic>Tcf7l2</jats:italic> was selectively ablated from mature adipocytes in C57BL/6J mice using an adiponectin promoter-driven <jats:italic>Cre</jats:italic> recombinase to recombine alleles floxed at exon 1 of the <jats:italic>Tcf7l2</jats:italic> gene. Mice lacking <jats:italic>Tcf7l2</jats:italic> in mature adipocytes displayed normal body weight. Male mice exhibited normal glucose homeostasis at eight weeks of age. Male heterozygote knockout mice (aTCF7L2het) exhibited impaired glucose tolerance (AUC increased 1.14 ± 0.04 -fold, p=0.03), as assessed by intraperitoneal glucose tolerance test, and changes in fat mass at 16 weeks (increased by 1.4 ± 0.09-fold, p=0.007). Homozygote knockout mice exhibited impaired oral glucose tolerance at 16 weeks of age (AUC increased 2.15 ± 0.15-fold, p=0.0001). Islets of Langerhans exhibited impaired glucose-stimulated insulin secretion <jats:italic>in vitro</jats:italic> (decreased 0.54 ± 0.13-fold aTCF7L2KO vs control, p=0.02), but no changes in <jats:italic>in vivo</jats:italic> glucose-stimulated insulin secretion. Female mice in which one or two alleles of the <jats:italic>Tcf7l2</jats:italic> gene was knocked out in adipocytes displayed no changes in glucose tolerance, insulin sensitivity or insulin secretion. Plasma levels of glucagon-like peptide-1 and gastric inhibitory polypeptide were lowered in knockout mice (decreased 0.57 ± 0.03-fold and 0.41 ± 0.12-fold
Martinez-Sanchez A, Lazzarano S, Sharma E, et al., 2020, High-Throughput Identification of MiR-145 Targets in Human Articular Chondrocytes, LIFE-BASEL, Vol: 10
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- Citations: 6
Georgiadou E, Haythorne E, Dickerson MT, et al., 2020, The pore-forming subunit MCU of the mitochondrial Ca2+ uniporter is required for normal glucose-stimulated insulin secretion in vitro and in vivo in mice, Diabetologia, Vol: 63, Pages: 1368-1381, ISSN: 0012-186X
Aims/hypothesisMitochondrial oxidative metabolism is central to glucose-stimulated insulin secretion (GSIS). Whether Ca2+ uptake into pancreatic beta cell mitochondria potentiates or antagonises this process is still a matter of debate. Although the mitochondrial Ca2+ importer (MCU) complex is thought to represent the main route for Ca2+ transport across the inner mitochondrial membrane, its role in beta cells has not previously been examined in vivo.MethodsHere, we inactivated the pore-forming subunit of the MCU, encoded by Mcu, selectively in mouse beta cells using Ins1Cre-mediated recombination. Whole or dissociated pancreatic islets were isolated and used for live beta cell fluorescence imaging of cytosolic or mitochondrial Ca2+ concentration and ATP production in response to increasing glucose concentrations. Electrophysiological recordings were also performed on whole islets. Serum and blood samples were collected to examine oral and i.p. glucose tolerance.ResultsGlucose-stimulated mitochondrial Ca2+ accumulation (p< 0.05), ATP production (p< 0.05) and insulin secretion (p< 0.01) were strongly inhibited in beta cell-specific Mcu-null (βMcu-KO) animals, in vitro, as compared with wild-type (WT) mice. Interestingly, cytosolic Ca2+ concentrations increased (p< 0.001), whereas mitochondrial membrane depolarisation improved in βMcu-KO animals. βMcu-KO mice displayed impaired in vivo insulin secretion at 5 min (p< 0.001) but not 15 min post-i.p. injection of glucose, whilst the opposite phenomenon was observed following an oral gavage at 5 min. Unexpectedly, glucose tolerance was improved (p< 0.05) in young βMcu-KO (<12 weeks), but not in older animals vs WT mice.Conclusions/interpretationMCU is crucial for mitochondrial Ca2+ uptake in pancreatic beta cells and is required for normal GSIS. The apparent compensatory mechanisms that maintain glucose tolerance in βMcu-KO mice remain
Clough TJ, Baxan N, Coakley EJ, et al., 2020, Synthesis and in vivo behaviour of an exendin-4-based MRI probe capable of beta-cell-dependent contrast enhancement in the pancreas, Dalton Transactions: an international journal of inorganic chemistry, Vol: 49, Pages: 4732-4740, ISSN: 1477-9226
Global rates of diabetes mellitus are increasing, and treatment of the disease consumes a growing proportion of healthcare spending across the world. Pancreatic β-cells, responsible for insulin production, decline in mass in type 1 and, to a more limited degree, in type 2 diabetes. However, the extent and rate of loss in both diseases differs between patients resulting in the need for the development of novel diagnostic tools, which could quantitatively assess changes in mass of β-cells over time and potentially lead to earlier diagnosis and improved treatments. Exendin-4, a potent analogue of glucagon-like-peptide 1 (GLP-1), binds to the receptor GLP-1R, whose expression is enriched in β-cells. GLP-1R has thus been used in the past as a means of targeting probes for a wide variety of imaging modalities to the endocrine pancreas. However, exendin-4 conjugates designed specifically for MRI contrast agents are an under-explored area. In the present work, the synthesis and characterization of an exendin-4-dota(ga)-Gd(III) complex, GdEx, is reported, along with its in vivo behaviour in healthy and in β-cell-depleted C57BL/6J mice. Compared to the ubiquitous probe, [Gd(dota)]−, GdEx shows selective uptake by the pancreas with a marked decrease in accumulation observed after the loss of β-cells elicited by deleting the microRNA processing enzyme, DICER. These results open up pathways towards the development of other targeted MRI contrast agents based on similar chemistry methodology.
Cheung R, Pizza G, Nguyen-Tu M-S, et al., 2019, Glucose-controlled miR-125b regulates beta cell function, 55th Annual Meeting of the European-Association-for-the-Study-of-Diabetes (EASD), Publisher: SPRINGER, Pages: S219-S219, ISSN: 0012-186X
Cheung R, Pizza G, Rolando DM, et al., 2019, miR-125b Is Regulated by Glucose via AMPK and Impairs β-Cell Function, 79th Scientific Sessions of the American-Diabetes-Association (ADA), Publisher: AMER DIABETES ASSOC, ISSN: 0012-1797
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- Citations: 3
Harris JP, Nguyen-Tu MS, Georgiadou E, et al., 2019, The impact of activating AMP-activated kinase (AMPK) on insulin secretion from the pancreatic beta cell, Publisher: WILEY, Pages: 41-41, ISSN: 0742-3071
Gharavy SNM, Hu M, Gadue P, et al., 2019, Roles for the Type 2 diabetes-associated genes <i>C2CD4A</i> and <i>C2CD4B</i> in the control of glucose homeostasis and insulin secretion, Publisher: WILEY, Pages: 43-43, ISSN: 0742-3071
Martinez-Sanchez A, Nguyen-Tu M-S, Cebola I, et al., 2018, MiR-184 expression is regulated by AMPK in pancreatic islets., FASEB Journal, Vol: 32, Pages: 2587-2600, ISSN: 0892-6638
AMPK is a critical energy sensor and target for widely used antidiabetic drugs. In β-cells, elevated glucose concentrations lower AMPK activity, and the ablation of both catalytic subunits (βAMPKdKO mice) impairs insulin secretion in vivo and β-cell identity. MicroRNAs (miRNAs) are small RNAs that silence gene expression that are essential for pancreatic β-cell function and identity and altered in diabetes. Here, we have explored the miRNAs acting downstream of AMPK in mouse and human β-cells. We identified 14 down-regulated and 9 up-regulated miRNAs in βAMPKdKO vs. control islets. Gene ontology analysis of targeted transcripts revealed enrichment in pathways important for β-cell function and identity. The most down-regulated miRNA was miR-184 (miR-184-3p), an important regulator of β-cell function and compensatory expansion that is controlled by glucose and reduced in diabetes. We demonstrate that AMPK is a potent regulator and an important mediator of the negative effects of glucose on miR-184 expression. Additionally, we reveal sexual dimorphism in miR-184 expression in mouse and human islets. Collectively, these data demonstrate that glucose-mediated changes in AMPK activity are central for the regulation of miR-184 and other miRNAs in islets and provide a link between energy status and gene expression in β-cells.-Martinez-Sanchez, A., Nguyen-Tu, M.-S., Cebola, I., Yavari, A., Marchetti, P., Piemonti, L., de Koning, E., Shapiro, A. M. J., Johnson, P., Sakamoto, K., Smith, D. M., Leclerc, I., Ashrafian, H., Ferrer, J., Rutter, G. A. MiR-184 expression is regulated by AMPK in pancreatic islets.
Gharavy NM, Li X, Leclerc I, et al., 2018, Roles for the Type 2 diabetes-associated genes <i>C2CD4A</i> and <i>C2CD4B</i> in the control of insulin secretion, Publisher: WILEY, Pages: 40-41, ISSN: 0742-3071
Martinez-Sanchez A, Nguyen-Tu MS, Cebola I, et al., 2018, Adenosine Monophosphate (AMP)-activated protein kinase (AMPK) regulates the expression of miR-184 and other miRNAs important for beta cell function, Publisher: WILEY, Pages: 48-48, ISSN: 0742-3071
Cheung R, Rolando D, Chabosseau P, et al., 2018, miR-125b is a new regulator of pancreatic beta cell function, Publisher: WILEY, Pages: 47-47, ISSN: 0742-3071
Martinez-Sanchez A, Pizza G, Marchetti P, et al., 2018, Glucose regulates miR-125b expression via AMP-activated protein kinase (AMPK), Publisher: WILEY, Pages: 49-49, ISSN: 0742-3071
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