Ignet

Gene Information

Gene symbol: TMEM27

Gene name: transmembrane protein 27

HGNC ID: 29437

Synonyms: NX17

Related Genes

#	Gene Symbol	Number of hits
1	APLP2	1 hits
2	BACE1	1 hits
3	BACE2	1 hits
4	HNF1A	1 hits
5	INS	1 hits
6	NAPA	1 hits
7	NSF	1 hits
8	SNAP23	1 hits
9	SNAP25	1 hits
10	SNAPIN	1 hits

Related Sentences

#	PMID	Sentence
1	16330323	The HNF-1 target collectrin controls insulin exocytosis by SNARE complex formation.
2	16330323	Overexpression of collectrin in rat insulinoma INS-1 cells or in the beta cells of transgenic mice enhanced glucose-stimulated insulin exocytosis, without affecting Ca(2+) influx.
3	16330323	Conversely, suppression of collectrin attenuated insulin secretion.
4	16330323	Collectrin bound to SNARE complexes by interacting with snapin, a SNAP-25 binding protein, and facilitated SNARE complex formation.
5	16330323	Therefore, collectrin is a regulator of SNARE complex function, which thereby controls insulin exocytosis.
6	16330323	The HNF-1 target collectrin controls insulin exocytosis by SNARE complex formation.
7	16330323	Overexpression of collectrin in rat insulinoma INS-1 cells or in the beta cells of transgenic mice enhanced glucose-stimulated insulin exocytosis, without affecting Ca(2+) influx.
8	16330323	Conversely, suppression of collectrin attenuated insulin secretion.
9	16330323	Collectrin bound to SNARE complexes by interacting with snapin, a SNAP-25 binding protein, and facilitated SNARE complex formation.
10	16330323	Therefore, collectrin is a regulator of SNARE complex function, which thereby controls insulin exocytosis.
11	16330323	The HNF-1 target collectrin controls insulin exocytosis by SNARE complex formation.
12	16330323	Overexpression of collectrin in rat insulinoma INS-1 cells or in the beta cells of transgenic mice enhanced glucose-stimulated insulin exocytosis, without affecting Ca(2+) influx.
13	16330323	Conversely, suppression of collectrin attenuated insulin secretion.
14	16330323	Collectrin bound to SNARE complexes by interacting with snapin, a SNAP-25 binding protein, and facilitated SNARE complex formation.
15	16330323	Therefore, collectrin is a regulator of SNARE complex function, which thereby controls insulin exocytosis.
16	16330323	The HNF-1 target collectrin controls insulin exocytosis by SNARE complex formation.
17	16330323	Overexpression of collectrin in rat insulinoma INS-1 cells or in the beta cells of transgenic mice enhanced glucose-stimulated insulin exocytosis, without affecting Ca(2+) influx.
18	16330323	Conversely, suppression of collectrin attenuated insulin secretion.
19	16330323	Collectrin bound to SNARE complexes by interacting with snapin, a SNAP-25 binding protein, and facilitated SNARE complex formation.
20	16330323	Therefore, collectrin is a regulator of SNARE complex function, which thereby controls insulin exocytosis.
21	16330323	The HNF-1 target collectrin controls insulin exocytosis by SNARE complex formation.
22	16330323	Overexpression of collectrin in rat insulinoma INS-1 cells or in the beta cells of transgenic mice enhanced glucose-stimulated insulin exocytosis, without affecting Ca(2+) influx.
23	16330323	Conversely, suppression of collectrin attenuated insulin secretion.
24	16330323	Collectrin bound to SNARE complexes by interacting with snapin, a SNAP-25 binding protein, and facilitated SNARE complex formation.
25	16330323	Therefore, collectrin is a regulator of SNARE complex function, which thereby controls insulin exocytosis.
26	17919177	Maturity-onset diabetes of the young (MODY) is a monogenic form of type 2 diabetes mellitus that is characterized by impairment of glucose-stimulated insulin secretion from pancreatic beta-cells.
27	17919177	We previously reported that heterozygous mutations of the hepatocyte nuclear factor (HNF)-1alpha gene cause a form of MODY (MODY3).
28	17919177	In addition, we have demonstrated that collectrin forms a complex with the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex by direct interaction with snapin, a protein that is thought to be involved in neurotransmission by binding to synaptosomal-associated protein, 25 KD (SNAP25).
29	17919177	Collectrin favours the formation of SNARE complexes and controls insulin exocytosis.
30	17919177	Maturity-onset diabetes of the young (MODY) is a monogenic form of type 2 diabetes mellitus that is characterized by impairment of glucose-stimulated insulin secretion from pancreatic beta-cells.
31	17919177	We previously reported that heterozygous mutations of the hepatocyte nuclear factor (HNF)-1alpha gene cause a form of MODY (MODY3).
32	17919177	In addition, we have demonstrated that collectrin forms a complex with the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex by direct interaction with snapin, a protein that is thought to be involved in neurotransmission by binding to synaptosomal-associated protein, 25 KD (SNAP25).
33	17919177	Collectrin favours the formation of SNARE complexes and controls insulin exocytosis.
34	19246514	Increased insulin sensitivity in mice lacking collectrin, a downstream target of HNF-1alpha.
35	19246514	Collectrin is a downstream target of the transcription factor hepatocyte nuclear factor-1alpha (HNF-1alpha), which is mutated in maturity-onset diabetes of the young subtype 3 (MODY3).
36	19246514	Evidence from transgenic mouse models with collectrin overexpression in pancreatic islets suggests divergent roles for collectrin in influencing beta-cell mass and insulin exocytosis.
37	19246514	However, we note that by 6 months of age, Tmem27(-/y) mice exhibit increased insulin sensitivity by IPITT and decreased adiposity by dual-energy x-ray absorptiometry scanning compared with wild-type.
38	19246514	Increased insulin sensitivity in mice lacking collectrin, a downstream target of HNF-1alpha.
39	19246514	Collectrin is a downstream target of the transcription factor hepatocyte nuclear factor-1alpha (HNF-1alpha), which is mutated in maturity-onset diabetes of the young subtype 3 (MODY3).
40	19246514	Evidence from transgenic mouse models with collectrin overexpression in pancreatic islets suggests divergent roles for collectrin in influencing beta-cell mass and insulin exocytosis.
41	19246514	However, we note that by 6 months of age, Tmem27(-/y) mice exhibit increased insulin sensitivity by IPITT and decreased adiposity by dual-energy x-ray absorptiometry scanning compared with wild-type.
42	19246514	Increased insulin sensitivity in mice lacking collectrin, a downstream target of HNF-1alpha.
43	19246514	Collectrin is a downstream target of the transcription factor hepatocyte nuclear factor-1alpha (HNF-1alpha), which is mutated in maturity-onset diabetes of the young subtype 3 (MODY3).
44	19246514	Evidence from transgenic mouse models with collectrin overexpression in pancreatic islets suggests divergent roles for collectrin in influencing beta-cell mass and insulin exocytosis.
45	19246514	However, we note that by 6 months of age, Tmem27(-/y) mice exhibit increased insulin sensitivity by IPITT and decreased adiposity by dual-energy x-ray absorptiometry scanning compared with wild-type.
46	19246514	Increased insulin sensitivity in mice lacking collectrin, a downstream target of HNF-1alpha.
47	19246514	Collectrin is a downstream target of the transcription factor hepatocyte nuclear factor-1alpha (HNF-1alpha), which is mutated in maturity-onset diabetes of the young subtype 3 (MODY3).
48	19246514	Evidence from transgenic mouse models with collectrin overexpression in pancreatic islets suggests divergent roles for collectrin in influencing beta-cell mass and insulin exocytosis.
49	19246514	However, we note that by 6 months of age, Tmem27(-/y) mice exhibit increased insulin sensitivity by IPITT and decreased adiposity by dual-energy x-ray absorptiometry scanning compared with wild-type.
50	21907142	Here we identified, through a siRNA screen, beta site amyloid precursor protein cleaving enzyme 2 (Bace2) as the sheddase of the proproliferative plasma membrane protein Tmem27 in murine and human β cells.
51	21907142	Mice with functionally inactive Bace2 and insulin-resistant mice treated with a newly identified Bace2 inhibitor both display augmented β cell mass and improved control of glucose homeostasis due to increased insulin levels.