Ignet

Gene Information

Gene symbol: BTG3

Gene name: BTG family, member 3

HGNC ID: 1132

Synonyms: ANA, tob55

Related Genes

#	Gene Symbol	Number of hits
1	ACOX1	1 hits
2	ATM	1 hits
3	AXPC1	1 hits
4	CALR	1 hits
5	CPT2	1 hits
6	FABP1	1 hits
7	FASN	1 hits
8	INS	1 hits
9	MPO	1 hits
10	PPARA	1 hits
11	SSB	1 hits
12	TBX1	1 hits
13	TG	1 hits
14	TPO	1 hits

Related Sentences

#	PMID	Sentence
1	3769971	Islet cell antibodies (ICA-IgG and complement-fixing-ICA), parietal cell antibodies (PCA), intestinal epithelial cell antibodies (IECA), thyroglobulin (TgA) and thyroid microsomal antibodies (MsA), antinuclear (ANA) and reticulin antibodies (RA), were studied in 55 insulin-dependent diabetic patients (30 males and 25 females), aged 2-19 years with diabetes from a few days up to 14 years.
2	3769971	In 58% of the diabetics one or more autoantibodies were found: ICA-IgG (31%), CF-ICA (16%), PCA (34%), TgA (9%), MsA (9%), ANA (13%), RA (2%).
3	3769971	ICA-IgG, CF-ICA, PCA, ANA were significantly more frequent in patients than in controls.
4	3769971	The frequency of ICA-IgG and CF-ICA was significantly higher during the first 3 years of disease than afterwards (P less than 0.001); a similar pattern was observed for PCA, TgA, MsA.
5	3769971	Of the 87 parents and 30 siblings screened for ICA-IgG, CF-ICA, PCA, IECA, TgA, MsA, ANA and RA, 42 (44%) had one or more autoantibodies, which were more frequent in females than in males.
6	3769971	Islet cell antibodies (ICA-IgG and complement-fixing-ICA), parietal cell antibodies (PCA), intestinal epithelial cell antibodies (IECA), thyroglobulin (TgA) and thyroid microsomal antibodies (MsA), antinuclear (ANA) and reticulin antibodies (RA), were studied in 55 insulin-dependent diabetic patients (30 males and 25 females), aged 2-19 years with diabetes from a few days up to 14 years.
7	3769971	In 58% of the diabetics one or more autoantibodies were found: ICA-IgG (31%), CF-ICA (16%), PCA (34%), TgA (9%), MsA (9%), ANA (13%), RA (2%).
8	3769971	ICA-IgG, CF-ICA, PCA, ANA were significantly more frequent in patients than in controls.
9	3769971	The frequency of ICA-IgG and CF-ICA was significantly higher during the first 3 years of disease than afterwards (P less than 0.001); a similar pattern was observed for PCA, TgA, MsA.
10	3769971	Of the 87 parents and 30 siblings screened for ICA-IgG, CF-ICA, PCA, IECA, TgA, MsA, ANA and RA, 42 (44%) had one or more autoantibodies, which were more frequent in females than in males.
11	3769971	Islet cell antibodies (ICA-IgG and complement-fixing-ICA), parietal cell antibodies (PCA), intestinal epithelial cell antibodies (IECA), thyroglobulin (TgA) and thyroid microsomal antibodies (MsA), antinuclear (ANA) and reticulin antibodies (RA), were studied in 55 insulin-dependent diabetic patients (30 males and 25 females), aged 2-19 years with diabetes from a few days up to 14 years.
12	3769971	In 58% of the diabetics one or more autoantibodies were found: ICA-IgG (31%), CF-ICA (16%), PCA (34%), TgA (9%), MsA (9%), ANA (13%), RA (2%).
13	3769971	ICA-IgG, CF-ICA, PCA, ANA were significantly more frequent in patients than in controls.
14	3769971	The frequency of ICA-IgG and CF-ICA was significantly higher during the first 3 years of disease than afterwards (P less than 0.001); a similar pattern was observed for PCA, TgA, MsA.
15	3769971	Of the 87 parents and 30 siblings screened for ICA-IgG, CF-ICA, PCA, IECA, TgA, MsA, ANA and RA, 42 (44%) had one or more autoantibodies, which were more frequent in females than in males.
16	3769971	Islet cell antibodies (ICA-IgG and complement-fixing-ICA), parietal cell antibodies (PCA), intestinal epithelial cell antibodies (IECA), thyroglobulin (TgA) and thyroid microsomal antibodies (MsA), antinuclear (ANA) and reticulin antibodies (RA), were studied in 55 insulin-dependent diabetic patients (30 males and 25 females), aged 2-19 years with diabetes from a few days up to 14 years.
17	3769971	In 58% of the diabetics one or more autoantibodies were found: ICA-IgG (31%), CF-ICA (16%), PCA (34%), TgA (9%), MsA (9%), ANA (13%), RA (2%).
18	3769971	ICA-IgG, CF-ICA, PCA, ANA were significantly more frequent in patients than in controls.
19	3769971	The frequency of ICA-IgG and CF-ICA was significantly higher during the first 3 years of disease than afterwards (P less than 0.001); a similar pattern was observed for PCA, TgA, MsA.
20	3769971	Of the 87 parents and 30 siblings screened for ICA-IgG, CF-ICA, PCA, IECA, TgA, MsA, ANA and RA, 42 (44%) had one or more autoantibodies, which were more frequent in females than in males.
21	6393433	ATA and ANA were detected in 8.9% and 1%, respectively.
22	6393433	Pancreatic isles cell surface antibodies (ICsA), ATA and ANA were studied simultaneously.
23	6393433	ATA and ANA were detected in 8.9% and 1%, respectively.
24	6393433	Pancreatic isles cell surface antibodies (ICsA), ATA and ANA were studied simultaneously.
25	20084921	ANA (screen), dsDNA, SS-A, SS-B, Scl-70, LKM-1, MPO and M2 autoantibodies have been investigated by ELISA (Euroimmun, Germany), while ANCA, AMA and ASMA antibodies by indirect immunofluorescence (IMMCO, NY) methods.
26	22844291	The targets of ANA in patients with autoimmune pancreatitis do not appear to be similar to those found in other rheumatological diseases, as dsDNA, SS-A, and SS-B are not frequently recognized by AIP-related ANA.
27	22844291	Further studies have focused on the identification of pancreas-specific autoantigens and reported significant reactivity to lactoferrin, carbonic anhydrase, pancreas secretory trypsin inhibitor, amylase-alpha, heat-shock protein, and plasminogen-binding protein.
28	23533380	Inhibitors of Fatty Acid Synthesis Induce PPAR α -Regulated Fatty Acid β -Oxidative Genes: Synergistic Roles of L-FABP and Glucose.
29	23533380	While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone.
30	23533380	Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor- α (PPAR α ) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity.
31	23533380	Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure.
32	23533380	High (20 mM) but not physiological (6 mM) glucose conferred on both TOFA and C75 the ability to induce PPAR α transcription of the fatty acid β -oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice.
33	23533380	However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose.
34	23533380	These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPAR α in the context of high glucose at levels similar to those in uncontrolled diabetes.
35	23533380	Inhibitors of Fatty Acid Synthesis Induce PPAR α -Regulated Fatty Acid β -Oxidative Genes: Synergistic Roles of L-FABP and Glucose.
36	23533380	While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone.
37	23533380	Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor- α (PPAR α ) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity.
38	23533380	Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure.
39	23533380	High (20 mM) but not physiological (6 mM) glucose conferred on both TOFA and C75 the ability to induce PPAR α transcription of the fatty acid β -oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice.
40	23533380	However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose.
41	23533380	These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPAR α in the context of high glucose at levels similar to those in uncontrolled diabetes.
42	23533380	Inhibitors of Fatty Acid Synthesis Induce PPAR α -Regulated Fatty Acid β -Oxidative Genes: Synergistic Roles of L-FABP and Glucose.
43	23533380	While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone.
44	23533380	Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor- α (PPAR α ) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity.
45	23533380	Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure.
46	23533380	High (20 mM) but not physiological (6 mM) glucose conferred on both TOFA and C75 the ability to induce PPAR α transcription of the fatty acid β -oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice.
47	23533380	However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose.
48	23533380	These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPAR α in the context of high glucose at levels similar to those in uncontrolled diabetes.
49	23533380	Inhibitors of Fatty Acid Synthesis Induce PPAR α -Regulated Fatty Acid β -Oxidative Genes: Synergistic Roles of L-FABP and Glucose.
50	23533380	While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone.
51	23533380	Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor- α (PPAR α ) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity.
52	23533380	Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure.
53	23533380	High (20 mM) but not physiological (6 mM) glucose conferred on both TOFA and C75 the ability to induce PPAR α transcription of the fatty acid β -oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice.
54	23533380	However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose.
55	23533380	These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPAR α in the context of high glucose at levels similar to those in uncontrolled diabetes.
56	23533380	Inhibitors of Fatty Acid Synthesis Induce PPAR α -Regulated Fatty Acid β -Oxidative Genes: Synergistic Roles of L-FABP and Glucose.
57	23533380	While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone.
58	23533380	Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor- α (PPAR α ) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity.
59	23533380	Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure.
60	23533380	High (20 mM) but not physiological (6 mM) glucose conferred on both TOFA and C75 the ability to induce PPAR α transcription of the fatty acid β -oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice.
61	23533380	However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose.
62	23533380	These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPAR α in the context of high glucose at levels similar to those in uncontrolled diabetes.
63	23533380	Inhibitors of Fatty Acid Synthesis Induce PPAR α -Regulated Fatty Acid β -Oxidative Genes: Synergistic Roles of L-FABP and Glucose.
64	23533380	While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone.
65	23533380	Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor- α (PPAR α ) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity.
66	23533380	Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure.
67	23533380	High (20 mM) but not physiological (6 mM) glucose conferred on both TOFA and C75 the ability to induce PPAR α transcription of the fatty acid β -oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice.
68	23533380	However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose.
69	23533380	These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPAR α in the context of high glucose at levels similar to those in uncontrolled diabetes.