Ignet

Gene Information

Gene symbol: FAM3B

Gene name: family with sequence similarity 3, member B

HGNC ID: 1253

Synonyms: D21M16SJHU19e, PRED44, 2-21, ORF9, C21orf76

Related Genes

#	Gene Symbol	Number of hits
1	CASP3	1 hits
2	IFNG	1 hits
3	IL1B	1 hits
4	INS	1 hits
5	IRS1	1 hits
6	PIK3CA	1 hits
7	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	12941769	Pancreatic-derived factor (FAM3B), a novel islet cytokine, induces apoptosis of insulin-secreting beta-cells.
2	12941769	PANDER protein was present in alpha- and beta-cells of pancreatic islets, insulin-secreting beta-TC3 cells, and glucagon-secreting alpha-TC cells.
3	12941769	However, PANDER activated caspase-3.
4	12941769	Pancreatic-derived factor (FAM3B), a novel islet cytokine, induces apoptosis of insulin-secreting beta-cells.
5	12941769	PANDER protein was present in alpha- and beta-cells of pancreatic islets, insulin-secreting beta-TC3 cells, and glucagon-secreting alpha-TC cells.
6	12941769	However, PANDER activated caspase-3.
7	12941769	Pancreatic-derived factor (FAM3B), a novel islet cytokine, induces apoptosis of insulin-secreting beta-cells.
8	12941769	PANDER protein was present in alpha- and beta-cells of pancreatic islets, insulin-secreting beta-TC3 cells, and glucagon-secreting alpha-TC cells.
9	12941769	However, PANDER activated caspase-3.
10	16006032	Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells.
11	16006032	PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy.
12	16006032	Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls.
13	16006032	IL-1beta or TNFalpha alone had no effect.
14	16006032	Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone.
15	16006032	Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death.
16	16006032	Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells.
17	16006032	PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy.
18	16006032	Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls.
19	16006032	IL-1beta or TNFalpha alone had no effect.
20	16006032	Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone.
21	16006032	Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death.
22	16006032	Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells.
23	16006032	PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy.
24	16006032	Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls.
25	16006032	IL-1beta or TNFalpha alone had no effect.
26	16006032	Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone.
27	16006032	Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death.
28	16006032	Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells.
29	16006032	PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy.
30	16006032	Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls.
31	16006032	IL-1beta or TNFalpha alone had no effect.
32	16006032	Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone.
33	16006032	Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death.
34	16006032	Interferon-gamma-induced regulation of the pancreatic derived cytokine FAM3B in islets and insulin-secreting betaTC3 cells.
35	16006032	PANDER is localized to insulin-containing granules-based on confocal microscopy and immunogold electron microscopy.
36	16006032	Using real-time reverse transcription-polymerase chain reaction, treatment of betaTC3 cells with IL-1beta + TNFalpha + IFNgamma induced a significant seven-fold increase in PANDER mRNA expression (n = 3; p < 0.01 at 24 h, p < 0.05 at 48 h), while IFNgamma alone caused a 3.2-fold increase (n = 3; p < 0.01 at 24 h) compared to unstimulated and time-matched vehicle controls.
37	16006032	IL-1beta or TNFalpha alone had no effect.
38	16006032	Under those conditions, a similar up-regulation was also observed in mouse islet cells, with increases in PANDER mRNA of 5.9-fold and 5.0-fold after treatment with IL-1beta + TNFalpha + IFNgamma or IFNgamma alone.
39	16006032	Because PANDER mRNA expression is up-regulated by IFNgamma, a cytokine implicated in the pathogenesis of type 1 diabetes, PANDER may contribute to the pathogenesis of beta-cell death.
40	16114871	Structure-function studies of PANDER, an islet specific cytokine inducing cell death of insulin-secreting beta cells.
41	16114871	PANDER (pancreatic derived factor, FAM3B) is a novel cytokine, present in insulin secretory granules, that induces apoptosis of alpha and beta cells of mouse, rat, and human islets in a dose- and time-dependent manner, and may be implicated in diabetes.
42	16114871	Finally, the region between Cys91 and Phe152 constitutes the active part of PANDER, based on the demonstration that mutants with truncation of helix B or C caused decreased beta-cell death and did not inhibit insulin secretion, as compared to wild-type PANDER.
43	16114871	Structure-function studies of PANDER, an islet specific cytokine inducing cell death of insulin-secreting beta cells.
44	16114871	PANDER (pancreatic derived factor, FAM3B) is a novel cytokine, present in insulin secretory granules, that induces apoptosis of alpha and beta cells of mouse, rat, and human islets in a dose- and time-dependent manner, and may be implicated in diabetes.
45	16114871	Finally, the region between Cys91 and Phe152 constitutes the active part of PANDER, based on the demonstration that mutants with truncation of helix B or C caused decreased beta-cell death and did not inhibit insulin secretion, as compared to wild-type PANDER.
46	16114871	Structure-function studies of PANDER, an islet specific cytokine inducing cell death of insulin-secreting beta cells.
47	16114871	PANDER (pancreatic derived factor, FAM3B) is a novel cytokine, present in insulin secretory granules, that induces apoptosis of alpha and beta cells of mouse, rat, and human islets in a dose- and time-dependent manner, and may be implicated in diabetes.
48	16114871	Finally, the region between Cys91 and Phe152 constitutes the active part of PANDER, based on the demonstration that mutants with truncation of helix B or C caused decreased beta-cell death and did not inhibit insulin secretion, as compared to wild-type PANDER.
49	16249448	In this study, we investigated whether PANDER is secreted by pancreatic alpha- and beta-cells and whether PANDER secretion is regulated by glucose and other insulin secretagogues.
50	16249448	In mouse-derived insulin-secreting beta-TC3 cells, PANDER secretion in the presence of stimulatory concentrations of glucose was 2.8 +/- 0.4-fold higher (P < 0.05) than without glucose.
51	16249448	An L-type Ca2+ channel inhibitor, nifedipine, completely blocked both glucose- or KCl-induced insulin and PANDER secretion.
52	16249448	In conclusion, we found that 1) PANDER is secreted from both pancreatic alpha- and beta-cells, 2) glucose stimulates PANDER secretion dose dependently in beta-cell lines and primary islets but not in alpha-cells, 3) PANDER is likely cosecreted with insulin via the same regulatory mechanisms, and 4) structure and conformation is vital for PANDER secretion.
53	16249448	In this study, we investigated whether PANDER is secreted by pancreatic alpha- and beta-cells and whether PANDER secretion is regulated by glucose and other insulin secretagogues.
54	16249448	In mouse-derived insulin-secreting beta-TC3 cells, PANDER secretion in the presence of stimulatory concentrations of glucose was 2.8 +/- 0.4-fold higher (P < 0.05) than without glucose.
55	16249448	An L-type Ca2+ channel inhibitor, nifedipine, completely blocked both glucose- or KCl-induced insulin and PANDER secretion.
56	16249448	In conclusion, we found that 1) PANDER is secreted from both pancreatic alpha- and beta-cells, 2) glucose stimulates PANDER secretion dose dependently in beta-cell lines and primary islets but not in alpha-cells, 3) PANDER is likely cosecreted with insulin via the same regulatory mechanisms, and 4) structure and conformation is vital for PANDER secretion.
57	16249448	In this study, we investigated whether PANDER is secreted by pancreatic alpha- and beta-cells and whether PANDER secretion is regulated by glucose and other insulin secretagogues.
58	16249448	In mouse-derived insulin-secreting beta-TC3 cells, PANDER secretion in the presence of stimulatory concentrations of glucose was 2.8 +/- 0.4-fold higher (P < 0.05) than without glucose.
59	16249448	An L-type Ca2+ channel inhibitor, nifedipine, completely blocked both glucose- or KCl-induced insulin and PANDER secretion.
60	16249448	In conclusion, we found that 1) PANDER is secreted from both pancreatic alpha- and beta-cells, 2) glucose stimulates PANDER secretion dose dependently in beta-cell lines and primary islets but not in alpha-cells, 3) PANDER is likely cosecreted with insulin via the same regulatory mechanisms, and 4) structure and conformation is vital for PANDER secretion.
61	16249448	In this study, we investigated whether PANDER is secreted by pancreatic alpha- and beta-cells and whether PANDER secretion is regulated by glucose and other insulin secretagogues.
62	16249448	In mouse-derived insulin-secreting beta-TC3 cells, PANDER secretion in the presence of stimulatory concentrations of glucose was 2.8 +/- 0.4-fold higher (P < 0.05) than without glucose.
63	16249448	An L-type Ca2+ channel inhibitor, nifedipine, completely blocked both glucose- or KCl-induced insulin and PANDER secretion.
64	16249448	In conclusion, we found that 1) PANDER is secreted from both pancreatic alpha- and beta-cells, 2) glucose stimulates PANDER secretion dose dependently in beta-cell lines and primary islets but not in alpha-cells, 3) PANDER is likely cosecreted with insulin via the same regulatory mechanisms, and 4) structure and conformation is vital for PANDER secretion.
65	19683528	PANDER binds to the liver cell membrane and inhibits insulin signaling in HepG2 cells.
66	19683528	PANDER is a cytokine co-secreted with insulin from islet beta-cells.
67	19683528	In HepG2 cells, pre-treatment with PANDER ranging from 4 pM to 4 nM for 8h resulted in a maximal inhibition of insulin-stimulated activation of insulin receptor and insulin receptor substrate 1 by 52% and 63%, respectively.
68	19683528	Moreover, PANDER treatment also reduced insulin-stimulated PI3K and pAkt levels by 55% and 48%, respectively.
69	19683528	In summary, we have identified the liver as a novel target for PANDER, and PANDER may be involved in the progression of diabetes by regulating hepatic insulin signaling pathways.
70	19683528	PANDER binds to the liver cell membrane and inhibits insulin signaling in HepG2 cells.
71	19683528	PANDER is a cytokine co-secreted with insulin from islet beta-cells.
72	19683528	In HepG2 cells, pre-treatment with PANDER ranging from 4 pM to 4 nM for 8h resulted in a maximal inhibition of insulin-stimulated activation of insulin receptor and insulin receptor substrate 1 by 52% and 63%, respectively.
73	19683528	Moreover, PANDER treatment also reduced insulin-stimulated PI3K and pAkt levels by 55% and 48%, respectively.
74	19683528	In summary, we have identified the liver as a novel target for PANDER, and PANDER may be involved in the progression of diabetes by regulating hepatic insulin signaling pathways.
75	19683528	PANDER binds to the liver cell membrane and inhibits insulin signaling in HepG2 cells.
76	19683528	PANDER is a cytokine co-secreted with insulin from islet beta-cells.
77	19683528	In HepG2 cells, pre-treatment with PANDER ranging from 4 pM to 4 nM for 8h resulted in a maximal inhibition of insulin-stimulated activation of insulin receptor and insulin receptor substrate 1 by 52% and 63%, respectively.
78	19683528	Moreover, PANDER treatment also reduced insulin-stimulated PI3K and pAkt levels by 55% and 48%, respectively.
79	19683528	In summary, we have identified the liver as a novel target for PANDER, and PANDER may be involved in the progression of diabetes by regulating hepatic insulin signaling pathways.
80	19683528	PANDER binds to the liver cell membrane and inhibits insulin signaling in HepG2 cells.
81	19683528	PANDER is a cytokine co-secreted with insulin from islet beta-cells.
82	19683528	In HepG2 cells, pre-treatment with PANDER ranging from 4 pM to 4 nM for 8h resulted in a maximal inhibition of insulin-stimulated activation of insulin receptor and insulin receptor substrate 1 by 52% and 63%, respectively.
83	19683528	Moreover, PANDER treatment also reduced insulin-stimulated PI3K and pAkt levels by 55% and 48%, respectively.
84	19683528	In summary, we have identified the liver as a novel target for PANDER, and PANDER may be involved in the progression of diabetes by regulating hepatic insulin signaling pathways.
85	19683528	PANDER binds to the liver cell membrane and inhibits insulin signaling in HepG2 cells.
86	19683528	PANDER is a cytokine co-secreted with insulin from islet beta-cells.
87	19683528	In HepG2 cells, pre-treatment with PANDER ranging from 4 pM to 4 nM for 8h resulted in a maximal inhibition of insulin-stimulated activation of insulin receptor and insulin receptor substrate 1 by 52% and 63%, respectively.
88	19683528	Moreover, PANDER treatment also reduced insulin-stimulated PI3K and pAkt levels by 55% and 48%, respectively.
89	19683528	In summary, we have identified the liver as a novel target for PANDER, and PANDER may be involved in the progression of diabetes by regulating hepatic insulin signaling pathways.