Ignet

Gene Information

Gene symbol: SFTPA2B

Gene name: surfactant, pulmonary-associated protein A2B

HGNC ID: 23441

Related Genes

#	Gene Symbol	Number of hits
1	APOE	1 hits
2	EGF	1 hits
3	IGF1	1 hits
4	INS	1 hits
5	SFTPA1	1 hits
6	SFTPA1B	1 hits
7	SFTPB	1 hits
8	SFTPC	1 hits

Related Sentences

#	PMID	Sentence
1	1386745	Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats.
2	1386745	Tissues from fetuses and neonates of control and streptozotocin (STZ)-treated Sprague-Dawley rats were used to study the content and distribution of the hydrophobic surfactant protein B (SP-B) and the mRNAs for SP-B and SP-C using immunohistochemistry, RNA blotting, and tissue in situ hybridization.
3	1386745	Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age.
4	1386745	In fetal lungs from the STZ group, SP-B and SP-C mRNA also showed an increase with advancing gestational age, but the levels were decreased compared with controls at fetal days 18, 20, and 21 (P less than 0.05).
5	1386745	The difference between the STZ and control groups, in both protein (SP-B) and mRNA (SP-B and SP-C), diminished with advancing fetal age but remained significant up to fetal day 21.
6	1386745	Delayed hydrophobic surfactant protein (SP-B, SP-C) expression in fetuses of streptozotocin-treated rats.
7	1386745	Tissues from fetuses and neonates of control and streptozotocin (STZ)-treated Sprague-Dawley rats were used to study the content and distribution of the hydrophobic surfactant protein B (SP-B) and the mRNAs for SP-B and SP-C using immunohistochemistry, RNA blotting, and tissue in situ hybridization.
8	1386745	Both SP-B and SP-C mRNA were detectable at fetal day 18 in the control group and increased with advancing gestational age.
9	1386745	In fetal lungs from the STZ group, SP-B and SP-C mRNA also showed an increase with advancing gestational age, but the levels were decreased compared with controls at fetal days 18, 20, and 21 (P less than 0.05).
10	1386745	The difference between the STZ and control groups, in both protein (SP-B) and mRNA (SP-B and SP-C), diminished with advancing fetal age but remained significant up to fetal day 21.
11	1533098	The content and distribution of the 26-to 38-kDa surfactant protein (SP-A) and its mRNA were determined in fetuses of control and streptozotocin (STZ)-treated Sprague-Dawley rats using immunohistochemistry, RNA blotting, and in situ hybridization.
12	1540394	Overexpression of pulmonary surfactant apoprotein A mRNA in alveolar type II cells and nonciliated bronchiolar (Clara) epithelial cells in streptozotocin-induced diabetic rats demonstrated by in situ hybridization.
13	1540394	The most abundant surfactant protein is termed surfactant apoprotein A (SP-A).
14	1540394	We have examined the expression and localization of SP-A mRNA in streptozotocin-induced diabetic rats by in situ hybridization using a specific rat cDNA probe.
15	1540394	Immunohistostaining of SP-A in diabetic lungs was weak in alveolar type II cells.
16	1540394	However, by autoradiographs of in situ hybridization, compared with the control lungs, a larger number of silver grains for the SP-A mRNA were shown in alveolar type II cells and also in some bronchiolar epithelial (Clara) cells from the diabetic lungs.
17	1540394	These results were confirmed by measurement of the SP-A content and by Northern blot analysis.
18	1540394	The present study demonstrates an overexpression of SP-A mRNA despite the ultrastructural changes in the endoplasmic reticulum of alveolar type II cells in the diabetic lungs, which will provide new information on the regulatory mechanism of SP-A gene expression.
19	7917308	Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization.
20	7917308	We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA.
21	7917308	In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs.
22	7917308	Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs.
23	7917308	In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly.
24	7917308	Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.
25	7917308	Differential expressions of surfactant protein SP-A, SP-B, and SP-C mRNAs in rats with streptozotocin-induced diabetes demonstrated by in situ hybridization.
26	7917308	We have previously demonstrated by in situ hybridization and Northern blot analysis that alveolar type II cells and nonciliated bronchiolar epithelial (Clara) cells in lungs of rats with diabetes have decreased surfactant protein A (SP-A) but increased mRNA.
27	7917308	In the present study, we have examined the mRNA expression and localization of two hydrophobic surfactant proteins, SP-B and SP-C, and have compared them with SP-A mRNA levels and cellular localization in streptozotocin-induced diabetic lungs.
28	7917308	Ten weeks after injection, higher numbers of silver grains representing SP-A and SP-B mRNAs were observed in alveolar type II cells of diabetic lungs, compared with control lungs.
29	7917308	In contrast, in bronchiolar epithelial cells of diabetic lungs, the relative abundance of silver grains for SP-A mRNA increased approximately 2-fold above controls, while SP-B mRNA decreased slightly.
30	7917308	Taken together, there is differential expression in the level of SP-A, SP-B, and SP-C mRNAs in both alveolar and bronchiolar epithelial cells from diabetic lungs when compared with control lungs.
31	8048547	Exposure of explants of 18-day fetal rat lung to Na butyrate resulted in a decrease in surfactant protein A (SP-A) mRNA concentration to 7% of control after 6 h and to 18% of control after 24 h.
32	8048547	The effects on SP-B mRNA were similar to those on SP-A, but quantitatively less.
33	8825794	Changes in surfactant protein A mRNA levels in a rat model of insulin-treated diabetic pregnancy.
34	8825794	In this study, we measured fetal lung surfactant-associated protein A (SP-A) mRNA from diabetic rats treated with insulin by daily injection or osmotic pump.
35	8825794	Fetal lung SP-A mRNA levels were affected by the timing, length, and effectiveness of insulin treatment.
36	8825794	Although levels from all treatment groups were still less than control values, insulin treatment during the last 5 or 10 d of pregnancy resulted in a substantial increase in SP-A mRNA levels over those of from untreated diabetic pregnancies.
37	8825794	However, fetuses from the group with insulin treatment for the entire pregnancy showed decreases in fetal SP-A mRNA levels.
38	9767111	Insulin inhibits surfactant protein A and B gene expression in the H441 cell line.
39	9767111	We have shown previously that insulin inhibits the accumulation of mRNA for the surfactant-associated proteins A and B (SP-A and SP-B) in human fetal lung explants maintained in vitro.
40	9767111	To test the hypothesis that the inhibitory effects of insulin on the surfactant proteins are the result of a direct action of insulin on the lung epithelial cell, we evaluated the effects of insulin in the H441 cell line, a human pulmonary adenocarcinoma cell line that expresses SP-A and SP-B mRNA.
41	9767111	We observed that insulin treatment for 48 h decreased SP-A mRNA and protein levels in a concentration-dependent manner when compared to controls.
42	9767111	The inhibitory effect of insulin on SP-A mRNA levels was apparent as early as after 4 h of exposure.
43	9767111	SP-B mRNA levels were also significantly decreased by insulin in a concentration-dependent manner.
44	9767111	Insulin, at 2.5 microg/ml, inhibited SP-A gene transcription by approx. 67%, and inhibited SP-B gene transcription by about 32%.
45	9767111	There was no significant effect of insulin on SP-A or SP-B mRNA stability.
46	9767111	Thus, we have observed a pattern of insulin inhibition of SP-A and SP-B gene expression in the H441 lung epithelial cell line similar to that previously observed in human fetal lung explants, which are comprised of both epithelial and mesenchymal cells.
47	9767111	Our findings provide further evidence that insulin may delay fetal lung maturation by inhibiting SP-A and SP-B gene expression.
48	10639200	The immunoreactivity (IR) of EGF, which was quantified using a computerized image analysis system, appeared with increased intensity and was associated with a reduced intensity of surfactant protein A-IR.
49	12965092	Simultaneously, there was an increase in the mRNAs of the ACTH-receptor and of the steroid-synthesizing enzymes in the fetal adrenal gland of the older, hypoxemic fetuses.
50	12965092	Growth and maturation of the fetal lung might also have been affected, because of the increase in surfactant-protein A mRNA in the older, hypoxemic animals and the decrease in the insulin-like growth factor-I and its binding protein-5 mRNA in the younger, hypoxemic fetuses.
51	15293882	Surfactant protein A (SP-A) is a lung collectin with diverse immunoregulatory activities.
52	15293882	Bone marrow-derived DCs generated in the presence of SP-A fail to increase lipopolysaccharide-induced upregulation of major histocompatibility complex (MHC) class II and CD86 costimulatory molecule on DCs surface and behaves like "tolerogenic DCs".
53	18285549	Circulating surfactant protein A (SP-A), a marker of lung injury, is associated with insulin resistance.