General Information:

Id: 2,977
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
MODY, type VI - [OMIM]
Mus musculus
neuroD beta-CKO mouse: mouse in which neuroD is deleted in insulin-expressing cells
article
Reference: Gu C et al.(2010) Pancreatic beta cells require NeuroD to achieve and maintain functional maturity Cell Metab 11: 298-310 [PMID: 20374962]

Interaction Information:

Comment NeuroD, a transactivator of the insulin gene, is critical for development of the endocrine pancreas, and NeuroD mutations cause MODY6 in humans. To investigate the role of NeuroD in differentiated beta cells, mice in which neuroD is deleted in insulin-expressing cells were generated. These mice exhibit severe glucose intolerance.
Formal Description
Interaction-ID: 27106

gene/protein

NEUROD1

affects_activity of

Comment Mice in which neuroD is deleted in insulin-expressing cells are severely deficient in glucosestimulated insulin secretion (GSIS), resulting in glucose intolerance.
Formal Description
Interaction-ID: 27108
Comment Although the mutant mice had a higher fasting level of blood glucose, their ability to take up glucose was not significantly different from controls. This result indicates that mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) are not insulin resistant, further supporting the hypothesis that they are glucose intolerant owing to defective insulin secretion.
Formal Description
Interaction-ID: 27109

gene/protein

NEUROD1

NOT affects_activity of

disease

Insulin resistance

Comment Plasma glucagon levels were not significantly different in mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) versus control mice regardless of whether they were fed ad libitum, fasted for 5 hr, or fasted overnight for 16 hr. These results imply that aberrations in glucagon secretion do not account for the modest hyperglycemia of neuroD beta-CKO mice.
Formal Description
Interaction-ID: 27110

gene/protein

NEUROD1

NOT affects_activity of

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) and control mice had a similar amount of hepatic glucose-6-phosphatase (G6Pase) mRNA, an indicator of gluconeogenesis, when fasted overnight, suggesting that gluconeogenesis was equally stimulated in both cases. However, at 90 min after glucose injection, G6Pase mRNA fails to decrease in the mutant mice. Because insulin is a powerful inhibitor of G6Pase expression, the failure to downregulate G6Pase mRNA in neuroD beta-CKO mice is likely due to their severe insulin secretion defect. Therefore, in neuroD beta-CKO mice, sustained gluconeogenesis may exacerbate hyperglycemia during glucose challenge.
Formal Description
Interaction-ID: 27111

gene/protein

NEUROD1

NOT affects_expression of

gene/protein

G6PC

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) and control mice had a similar amount of hepatic glucose-6-phosphatase (G6Pase) mRNA, an indicator of gluconeogenesis, when fasted overnight, suggesting that gluconeogenesis was equally stimulated in both cases. However, at 90 min after glucose injection, G6Pase mRNA fails to decrease in the mutant mice. Because insulin is a powerful inhibitor of G6Pase expression, the failure to downregulate G6Pase mRNA in neuroD beta-CKO mice is likely due to their severe insulin secretion defect. Therefore, in neuroD beta-CKO mice, sustained gluconeogenesis may exacerbate hyperglycemia during glucose challenge.
Formal Description
Interaction-ID: 27112

gene/protein

NEUROD1

NOT affects_activity of

process

gluconeogenesis

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) and control mice had a similar amount of hepatic glucose-6-phosphatase (G6Pase) mRNA, an indicator of gluconeogenesis, when fasted overnight, suggesting that gluconeogenesis was equally stimulated in both cases. However, at 90 min after glucose injection, G6Pase mRNA fails to decrease in the mutant mice. Because insulin is a powerful inhibitor of G6Pase expression, the failure to downregulate G6Pase mRNA in neuroD beta-CKO mice is likely due to their severe insulin secretion defect. Therefore, in neuroD beta-CKO mice, sustained gluconeogenesis may exacerbate hyperglycemia during glucose challenge.
Formal Description
Interaction-ID: 27113

gene/protein

NEUROD1

affects_quantity of

complex/PPI

Insulin

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) and control mice had a similar amount of hepatic glucose-6-phosphatase (G6Pase) mRNA, an indicator of gluconeogenesis, when fasted overnight, suggesting that gluconeogenesis was equally stimulated in both cases. However, at 90 min after glucose injection, G6Pase mRNA fails to decrease in the mutant mice. Because insulin is a powerful inhibitor of G6Pase expression, the failure to downregulate G6Pase mRNA in neuroD beta-CKO mice is likely due to their severe insulin secretion defect. Therefore, in neuroD beta-CKO mice, sustained gluconeogenesis may exacerbate hyperglycemia during glucose challenge.
Formal Description
Interaction-ID: 27114

gene/protein

G6PC

increases_activity of

process

gluconeogenesis

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) and control mice had a similar amount of hepatic glucose-6-phosphatase (G6Pase) mRNA, an indicator of gluconeogenesis, when fasted overnight, suggesting that gluconeogenesis was equally stimulated in both cases. However, at 90 min after glucose injection, G6Pase mRNA fails to decrease in the mutant mice. Because insulin is a powerful inhibitor of G6Pase expression, the failure to downregulate G6Pase mRNA in neuroD beta-CKO mice is likely due to their severe insulin secretion defect. Therefore, in neuroD beta-CKO mice, sustained gluconeogenesis may exacerbate hyperglycemia during glucose challenge.
Formal Description
Interaction-ID: 27115

complex/PPI

Insulin

decreases_expression of

gene/protein

G6PC

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) and control mice had a similar amount of hepatic glucose-6-phosphatase (G6Pase) mRNA, an indicator of gluconeogenesis, when fasted overnight, suggesting that gluconeogenesis was equally stimulated in both cases. However, at 90 min after glucose injection, G6Pase mRNA fails to decrease in the mutant mice. Because insulin is a powerful inhibitor of G6Pase expression, the failure to downregulate G6Pase mRNA in neuroD beta-CKO mice is likely due to their severe insulin secretion defect. Therefore, in neuroD beta-CKO mice, sustained gluconeogenesis may exacerbate hyperglycemia during glucose challenge.
Formal Description
Interaction-ID: 27116

gene/protein

NEUROD1

affects_activity of

phenotype

hyperglycemia

Comment Mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice) have only half as much Glut-2 protein as controls.
Formal Description
Interaction-ID: 27117

gene/protein

NEUROD1

affects_quantity of

gene/protein

SLC2A2

Drugbank entries Show/Hide entries for SLC2A2
Comment Pdx-1, Nkx6.1, and MafA, all of which are beta cell transcription factors that are involved in the activation of insulin transcription and the regulation of insulin secretion, are unaffected by the absence of NeuroD. These results indicate that the defective GSIS observed in neuroD beta-CKO mice is not a secondary consequence of altered regulation of these transcription factors.
Formal Description
Interaction-ID: 27118

gene/protein

NEUROD1

NOT affects_activity of

gene/protein

PDX1

Comment Pdx-1, Nkx6.1, and MafA, all of which are beta cell transcription factors that are involved in the activation of insulin transcription and the regulation of insulin secretion, are unaffected by the absence of NeuroD. These results indicate that the defective GSIS observed in neuroD beta-CKO mice is not a secondary consequence of altered regulation of these transcription factors.
Formal Description
Interaction-ID: 27119

gene/protein

NEUROD1

NOT affects_activity of

gene/protein

NKX6-1

Comment Pdx-1, Nkx6.1, and MafA, all of which are beta cell transcription factors that are involved in the activation of insulin transcription and the regulation of insulin secretion, are unaffected by the absence of NeuroD. These results indicate that the defective GSIS observed in neuroD beta-CKO mice is not a secondary consequence of altered regulation of these transcription factors.
Formal Description
Interaction-ID: 27120

gene/protein

NEUROD1

NOT affects_activity of

gene/protein

MAFA

Comment Pdx-1, Nkx6.1, and MafA, all of which are beta cell transcription factors that are involved in the activation of insulin transcription and the regulation of insulin secretion, are unaffected by the absence of NeuroD. These results indicate that the defective GSIS observed in neuroD beta-CKO mice is not a secondary consequence of altered regulation of these transcription factors.
Formal Description
Interaction-ID: 27121

gene/protein

PDX1

increases_activity of

in pancreas, in pancreatic islets
Comment Pdx-1, Nkx6.1, and MafA, all of which are beta cell transcription factors that are involved in the activation of insulin transcription and the regulation of insulin secretion, are unaffected by the absence of NeuroD. These results indicate that the defective GSIS observed in neuroD beta-CKO mice is not a secondary consequence of altered regulation of these transcription factors.
Formal Description
Interaction-ID: 27122

gene/protein

NKX6-1

increases_activity of

in pancreas, in pancreatic islets
Comment Pdx-1, Nkx6.1, and MafA, all of which are beta cell transcription factors that are involved in the activation of insulin transcription and the regulation of insulin secretion, are unaffected by the absence of NeuroD. These results indicate that the defective GSIS observed in neuroD beta-CKO mice is not a secondary consequence of altered regulation of these transcription factors.
Formal Description
Interaction-ID: 27123

gene/protein

MAFA

increases_activity of

in pancreas, in pancreatic islets
Comment Deletion of NeuroD in differentiated beta cells does not cause increased apoptosis or proliferation, which is consistent with the observed normal islet area in these mice.
Formal Description
Interaction-ID: 27124

gene/protein

NEUROD1

NOT affects_activity of

in pancreas, in pancreatic islets
Comment Deletion of NeuroD in differentiated beta cells does not cause increased apoptosis or proliferation, which is consistent with the observed normal islet area in these mice.
Formal Description
Interaction-ID: 27125

gene/protein

NEUROD1

NOT affects_activity of

in pancreas, in pancreatic islets
Comment Rodents express two closely related insulin genes, ins1 and ins2. NeuroD is not required for ins2 expression in vivo but is necessary for ins1 expression.
Formal Description
Interaction-ID: 27126

gene/protein

NEUROD1

affects_expression of

gene/protein

INS

in rodents
Drugbank entries Show/Hide entries for INS
Comment Sur1, a regulatory subunit of the pancreatic KATP channel, has been shown to be a transcriptional target of NeuroD in vitro. Consistent with a defect in KATP channel function, neuroD beta-CKO islets respond poorly to glipizide, a sulfonylurea drug, by secreting only 0.22% of their insulin content versus 0.79% for control islets. There is no difference in the mRNA expression of the KATP channel gene (Kir6.2, kcnj11) or its regulatory subunit (Sur1, abcc8) between mutant and control islets, indicating that NeuroD does not regulate these genes at the level of transcription in vivo.
Formal Description
Interaction-ID: 27127

gene/protein

NEUROD1

affects_activity of

complex/PPI

ATP-sensitive potassium channel complex

Comment Sur1, a regulatory subunit of the pancreatic KATP channel, has been shown to be a transcriptional target of NeuroD in vitro. Consistent with a defect in KATP channel function, neuroD beta-CKO islets respond poorly to glipizide, a sulfonylurea drug, by secreting only 0.22% of their insulin content versus 0.79% for control islets. There is no difference in the mRNA expression of the KATP channel gene (Kir6.2, kcnj11) or its regulatory subunit (Sur1, abcc8) between mutant and control islets, indicating that NeuroD does not regulate these genes at the level of transcription in vivo.
Formal Description
Interaction-ID: 27128

gene/protein

NEUROD1

NOT affects_expression of

gene/protein

KCNJ11

Drugbank entries Show/Hide entries for KCNJ11
Comment Sur1, a regulatory subunit of the pancreatic KATP channel, has been shown to be a transcriptional target of NeuroD in vitro. Consistent with a defect in KATP channel function, neuroD beta-CKO islets respond poorly to glipizide, a sulfonylurea drug, by secreting only 0.22% of their insulin content versus 0.79% for control islets. There is no difference in the mRNA expression of the KATP channel gene (Kir6.2, kcnj11) or its regulatory subunit (Sur1, abcc8) between mutant and control islets, indicating that NeuroD does not regulate these genes at the level of transcription in vivo.
Formal Description
Interaction-ID: 27129

gene/protein

NEUROD1

NOT affects_expression of

gene/protein

ABCC8

Drugbank entries Show/Hide entries for ABCC8
Comment The expression of Piccolo (pclo) and Noc2 (rph3al) are both decreased in mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice). Pclo encodes a scaffold protein that is necessary for assembly of insulin secretion complexes that link KATP channels, L-type calcium channels, and insulin granules into functional units, and Noc2 is a Rab effector that is required for GSIS through its interaction with small monomeric GTPases.
Formal Description
Interaction-ID: 27130

gene/protein

NEUROD1

affects_expression of

gene/protein

PCLO

Comment The expression of Piccolo (pclo) and Noc2 (rph3al) are both decreased in mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice). Pclo encodes a scaffold protein that is necessary for assembly of insulin secretion complexes that link KATP channels, L-type calcium channels, and insulin granules into functional units, and Noc2 is a Rab effector that is required for GSIS through its interaction with small monomeric GTPases.
Formal Description
Interaction-ID: 27131

gene/protein

NEUROD1

affects_expression of

gene/protein

RPH3AL

Comment Adenyl cyclase activity, which is necessary for the conversion of ATP to cAMP, is inhibited by Neuropeptide Y (NPY), a hormone whose expression is normally decreased in islets after birth. NPY mRNA is significantly increased in islets of mutant mice in which neuroD is deleted in insulin-expressing cells (neuroD beta-CKO mice). The upregulation of NPY in the beta cells of neuroD beta-CKO mice may contribute to their observed GSIS defects by decreasing the level of cAMP.
Formal Description
Interaction-ID: 27132

gene/protein

NEUROD1

affects_expression of

gene/protein

NPY

Drugbank entries Show/Hide entries for NPY
Comment Expression of lactate dehydrogenase A (LDHA) was significantly altered in the adult neuroD beta-CKO islets. Normally, mature beta cells are different than most mammalian cell types in that they have an unusually low amount of lactate dehydrogenase (LDH). In contrast, fetal and neonatal beta cells have elevated amounts of LDHA and an increased rate of glycolysis. LDHA (ldha) mRNA and protein are increased dramatically in neuroD beta-CKO islets in both low glucose and high glucose.
Formal Description
Interaction-ID: 27133

gene/protein

NEUROD1

affects_expression of

gene/protein

LDHA

Drugbank entries Show/Hide entries for LDHA
Comment Expression of lactate dehydrogenase A (LDHA) was significantly altered in the adult neuroD beta-CKO islets. Normally, mature beta cells are different than most mammalian cell types in that they have an unusually low amount of lactate dehydrogenase (LDH). In contrast, fetal and neonatal beta cells have elevated amounts of LDHA and an increased rate of glycolysis. LDHA (ldha) mRNA and protein are increased dramatically in neuroD beta-CKO islets in both low glucose and high glucose.
Formal Description
Interaction-ID: 27134

gene/protein

NEUROD1

affects_activity of

Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27135

gene/protein

NEUROD1

affects_expression of

gene/protein

ALDOB

Drugbank entries Show/Hide entries for ALDOB
Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27136

gene/protein

NEUROD1

affects_expression of

gene/protein

PFKL

Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27137

gene/protein

NEUROD1

affects_expression of

gene/protein

TPI1

Drugbank entries Show/Hide entries for TPI1
Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27138

gene/protein

NEUROD1

affects_expression of

gene/protein

ENO1

Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27139

gene/protein

NEUROD1

affects_expression of

gene/protein

PKLR

Drugbank entries Show/Hide entries for PKLR
Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27140

gene/protein

NEUROD1

NOT affects_activity of

Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27141

gene/protein

NEUROD1

NOT affects_activity of

Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27142

gene/protein

NEUROD1

NOT affects_expression of

gene/protein

PDHA1

Drugbank entries Show/Hide entries for PDHA1
Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27143

gene/protein

NEUROD1

NOT affects_expression of

gene/protein

PDK1

Drugbank entries Show/Hide entries for PDK1
Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27144

gene/protein

NEUROD1

NOT affects_expression of

gene/protein

SDHC

Drugbank entries Show/Hide entries for SDHC
Comment NeuroD beta-CKO islets have elevated expression of several other glycolytic genes, including aldolase B, phosphofructokinase, liver form (PFKL), triose phosphate isomerase (TPI), enolase 1 (ENO1) and pyruvate kinase, liver, and RBC form (PKLR). These changes in gene expression suggest that glycolysis is enhanced in neuroD beta-CKO islets. In contrast, there is no significant difference in the expression of key genes whose products participate in pyruvate metabolism and oxidative phosphorylation in mitochondria, such as pyruvate dehydrogenase A1 (Pdha-1) and its regulatory protein pyruvate dehydrogenase kinase 1 (PDK1), succinate dehydrogenase C (SDHC), and ATP synthase (ATP6). Overall, the pattern of gene expression in neuroD beta-CKO islets is consistent with the increase in glycolysis that is characteristic of neonatal beta cells.
Formal Description
Interaction-ID: 27145

gene/protein

NEUROD1

NOT affects_expression of

gene/protein

MT-ATP6