Biomedical subjects

Y Ishimura

Publications and source records attributed to Y Ishimura.

At least 91 records · Page 5Linked to original sources

PubMed1994

Carbon monoxide as an endogenous modulator of hepatic vascular perfusion.

Carbon monoxide (CO) generated by heme oxygenase has recently been considered a neural messenger in brain. This observation prompted us to investigate whether CO participates in vascular regulation in the liver, another organ with high levels of heme oxygenase activity. In isolated perfused rat liver, submicromolar levels of CO were detectable in the effluent and were able to be suppressed by the administration of Zn protoporphyrin IX (1 microM), a potent inhibitor of heme oxygenase. Furthermore, zinc protoporphyrin IX (1 microM) promoted an increase in the perfusion pressure under the constant flow conditions. These changes were reversed by adding CO (2 microM) or a cGMP analogue 8-bromo-cGMP (1 microM) in the perfusate. The present findings indicate that CO can function as an endogenous modulator of vascular perfusion in the liver.

Animals↗

PubMed1994

Muscarinic receptor-mediated calcium efflux from cultured bovine adrenal chromaffin cells.

The effect of stimulation of the muscarinic receptor on Ca2+ mobilization in cultured bovine adrenal chromaffin cells was examined. Acetylcholine (ACh) increased the uptake of 45Ca2+ and [Ca2+]i whose levels decreased with time after reaching peaks. It also enhanced the efflux of 45Ca2+ from the cells. Its effect was inhibited by the specific muscarinic receptor antagonist atropine (Atr), but not by the nicotinic receptor antagonist hexamethonium (C6). The increase in muscarine (Mus)-stimulated 45Ca2+ efflux was reduced concentration-dependently by deprivation of extracellular Na+. These results suggest that muscarinic stimulation of the ACh receptor stimulates Na+/Ca2+ exchange in cultured bovine adrenal chromaffin cells.

Acetylcholine↗

PubMed1994

Mechanism of histamine-induced calcium efflux from cultured bovine adrenal chromaffin cells: possible involvement of an Na+/Ca2+ exchange mechanism.

The effect of stimulation of the histamine receptor on Ca2+ mobilization in cultured bovine adrenal chromaffin cells was examined. Histamine (10(-5) M) increased the intracellular free Ca2+ ([Ca2+]i) to a peak in the presence or absence of extracellular Ca2+, followed by decrease with time. Histamine (10(-8)-10(-5) M) also stimulated 45Ca2+ efflux from cultured bovine adrenal chromaffin cells in a concentration dependent manner. Its stimulatory effect on 45Ca2+ efflux was inhibited by the specific histamine H1 receptor antagonist mepyramine. The increase in histamine-stimulated 45Ca2+ efflux was inhibited by deprivation of extracellular Na+ and by the Na+/Ca2+ exchange inhibitor amiloride. In addition, histamine stimulated 22Na+ influx into the cells, and this action was inhibited by amiloride. These results suggest that stimulation of the histamine H1 receptor regulates Na+/Ca2+ exchange in cultured bovine adrenal chromaffin cells.

Adrenal Medulla↗

PubMed1994

Inhibition by ouabain of palytoxin-induced catecholamine secretion and calcium influx into cultured bovine adrenal chromaffin cells.

The effect of ouabain on palytoxin (PTX)-induced catecholamine secretion from cultured bovine adrenal chromaffin cells was examined in relation to its effect on calcium (Ca2+) influx into the cells. Ouabain showed concentration-dependent inhibition of catecholamine secretion induced by PTX. Ouabain also inhibited [45Ca]2+ influx induced by PTX, this inhibition being parallel with that of catecholamine secretion. The inhibitory effects of ouabain on PTX-induced catecholamine secretion and [45Ca]2+ influx were both overcome by increasing the concentrations of PTX, indicating that ouabain inhibited the actions of PTX in a competitive manner. These results suggest that the ouabain-sensitive (or-binding) site on the cell membrane might be the target site of action of PTX, which causes an increase in Ca2+ permeability and initiation of catecholamine secretion.

Acrylamides↗

PubMed1994

High-pressure flash photolysis study of hemoprotein: effects of substrate analogues on the recombination of carbon monoxide to cytochrome P450CAM.

The effects of camphor and camphor analogues on the CO recombination kinetics of ferrous cytochrome P450CAM (P450CAM) at 293 K have been studied as a function of hydrostatic pressure (0.1-200 MPa) by means of flash photolysis. At 0.1 MPa, the association rate constant (kon) for substrate-free P450CAM is 8.5 x 10(6) M-1 s-1. Measurements as a function of pressure lead to a determination of the activation volume (delta V not equal to) of +4 cm3 mol-1 for substrate-free protein. This positive delta V not equal to is interesting because the CO association reaction of various hemoproteins, such as myoglobin and hemoglobin, exhibit negative delta V not equal to values [Adachi, S., & Morishima, I. (1989) J. Biol. Chem. 264, 18896-18901; Unno, M., Ishimori, K., & Morishima, I. (1990) Biochemistry 29, 10199-10205]. The binding of d-camphor and some camphor analogues (d-fenchone, 3-endo-bromocamphor, and 3,3,5,5-tetramethylcyclohexanone) into the heme pocket strongly influences the kinetics, i.e., kon is reduced ((1-10) x 10(5) M-1 s-1) and delta V not equal to is altered to a negative value (-14 to -32 cm3 mol-1). The negative delta V not equal to suggests that the effects of camphor and these camphor analogues are due to an increase in the iron-ligand bond formation barrier. On the other hand, the binding of adamantane and norcamphor does not affect the kinetics. This result is particularly surprising because both substrate analogues are located in the immediate vicinity of the CO binding site.(ABSTRACT TRUNCATED AT 250 WORDS)

Camphor↗

PubMed1994

Evidence for compound I formation in the reaction of cytochrome P450cam with m-chloroperbenzoic acid.

During the reaction of m-chloroperbenzoate with low spin ferric form of cytochrome P450cam, the formation of at least four transient intermediates was detected by employing rapid scan absorption spectrometry. Among them, the first one which appeared within 10 msec after the start of reaction gave an absorption spectrum indistinguishable from that of compound I of chloroperoxidase, another thiolate-heme protein. The intermediate exhibited the major absorption maxima at 367 and 694 nm, while chloroperoxidase compound I is known to have the maxima at 367 and 688 nm. The shapes of the bands at 367 nm were very similar to each other. Based on these spectral similarities, we suggest that the intermediate found in this study is the compound I of cytochrome P450cam.

Camphor 5-Monooxygenase↗

PubMed1994

Effects of the potassium channel openers cromakalim and pinacidil on catecholamine secretion and calcium mobilization in cultured bovine adrenal chromaffin cells.

The effects of two K+ channel openers, cromakalim and pinacidil, on voltage-dependent and receptor-mediated catecholamine secretion and Ca2+ mobilization in bovine adrenal chromaffin cells were studied to determine the role of membrane K+ channels in the regulation of a Ca(2+)-dependent secretory process. Both cromakalim and pinacidil stimulated the efflux of 86Rb (used to monitor K+ permeability) from preloaded cells. Cromakalim and pinacidil did not affect the catecholamine secretion induced by excessive depolarization with 56 mM K+, but inhibited that induced by moderate depolarization with 31 mM K+ in a concentration-dependent manner (1 microM-100 microM). The 31 mM K(+)-induced 45Ca2+ influx and increase in intracellular free Ca2+ concentration [Ca2+]i were also inhibited by these agents at similar concentrations to those for inhibition of catecholamine secretion. Cromakalim and pinacidil inhibited catecholamine secretion, 45Ca2+ influx and increase in [Ca2+]i induced by stimulation of nicotinic acetylcholine (ACh) receptors with carbamylcholine. Furthermore, both cromakalim and pinacidil inhibited the increase in [Ca2+]i induced by carbamylcholine in the absence of extracellular Ca2+, which is thought to be mediated by muscarinic ACh receptors. On the other hand, they did not affect catecholamine secretion induced by Bay-K 8644, Ba2+, A23187, histamine or bradykinin. These results indicate that the K+ channel openers, cromakalim and pinacidil, selectively inhibit catecholamine secretion induced by moderate depolarization or by nicotinic ACh receptor stimulation by inhibiting Ca2+ influx and increase in [Ca2+]i. Furthermore, the results suggest that these K+ channel openers-sensitive membrane K+ channels are involved in the regulation of catecholamine secretion mainly indirectly through effects on the voltage-dependent membrane Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1994

Calcium efflux from cultured bovine adrenal chromaffin cells induced by bradykinin.

The effect of bradykinin on Ca2+ efflux from cultured bovine adrenal chromaffin cells was examined. Bradykinin enhanced the efflux of 45Ca2+ from the cells in a concentration dependent manner (10(-9)-10(-6) M). This effect was inhibited by a specific bradykinin B2-receptor antagonist, but not by a B1-receptor antagonist. Nifedipine, Co2+ and Cd2+ did not inhibit the bradykinin-stimulated 45Ca2+ efflux from the cells. 12-O-Tetradecanoyl phorbol 13-acetate, an activator of protein kinase C, also had no effect on the efflux of 45Ca2+ from the cells. The increase in bradykinin-stimulated 45Ca2+ efflux was reduced by removal of extracellular Na+. These results suggest that bradykinin stimulates Na+/Ca2+ exchange in cultured bovine adrenal chromaffin cells.

Acetylcholine↗

PubMed1994

Pathophysiologic significance of free and conjugated dopamines in congestive heart failure.

sulfoconjugated dopamine constitutes the major portion of circulating or excreted dopamine, but its physiologic significance is still unknown. To test whether conjugated dopamine serves as a source of free dopamine in response to acute stress, plasma concentrations of free and conjugated dopamine were measured during an acute exacerbation of heart failure. The plasma concentration of conjugated dopamine decreased significantly during the acute phase of heart failure, whereas that of free dopamine increased. The plasma concentration of free dopamine decreased, whereas the concentration of conjugated dopamine increased as heart failure improved. An infusion of dopamine increased the plasma concentration of conjugated dopamine, suggesting that at least part of the excess active dopamine was detoxified through conjugation. The results of these tests with both conjugated and free dopamine are interconvertible and indicate that conjugated dopamine can serve as a reservoir of active dopamine.

Adult↗

PubMed1994

Contribution of renal angiotensin II type I receptor to gene expressions in hypertension-induced renal injury.

Recent evidence indicates that transforming growth factor-beta 1 (TGF-beta 1) plays an important role in renal fibrosis via stimulation of extracellular matrix synthesis. The present study was undertaken to investigate the role of angiotensin II type I receptor (AT1 receptor) in hypertension-induced renal injury. Twenty-two-week-old stroke-prone spontaneously hypertensive rats (SHRSP), which had established hypertension and moderate renal damage, were orally given TCV-116, a selective non-peptide AT1 receptor antagonist (0.1, 1 or 10 mg/kg/day), enalapril (10 mg/kg/day) or vehicle once a day for 10 weeks. At the end point of the treatment, we examined renal function, the gene expressions of TGF-beta 1 and extracellular matrix components in the interstitium [collagen types I (COI) and III (COIII), fibronectin (FN)] and the basement membrane (COIV and laminin), and renal microscopic morphology in rats aged 32 weeks. In vehicle-treated 32 week-old SHRSP with renal dysfunction and nephrosclerosis, renal mRNA levels for TGF-beta 1, COI, COIII, FN, COIV were all several-fold higher than in WKY. Thus, renal TGF-beta 1 gene expression was enhanced in SHRSP, which may contribute to the increased renal expressions of COI, COIII, FN, COIV in SHRSP. Treatment with TCV-116 (0.1 mg/kg/day) in SHRSP, in spite of no reduction of blood pressure, decreased renal mRNA levels for TGF-beta 1, COI, COIII, FN, COIV, being accompanied by the significant decrease in urinary protein and albumin excretion, blood urea nitrogen and plasma creatinine. Treatment with TCV-116 (10 mg/kg/day) in SHRSP decreased mRNAs for TGF-beta 1, COI, COIII, FN and COIV to almost the same levels as WKY, being associated with normalization of urinary protein and albumin excretion and the prevention of nephrosclerosis, as judged by microscopic histological observations. On the other hand, the effects of enalapril (10 mg/kg/day) on the above mentioned mRNA levels, renal function and renal morphology were weaker than those of TCV-116 (10 mg/kg/day) and were as much as TCV-116 (1 mg/kg/day). These results suggest that independently of hypotensive action, AT1 receptor antagonist has a potent renal protective effect by inhibiting the gene expression of renal TGF-beta 1 and extracellular matrix components.

Angiotensin II↗

PubMed1994

Role of angiotensin II in renal injury of deoxycorticosterone acetate-salt hypertensive rats.

To investigate the role of angiotensin II (Ang II) in hypertension-induced tissue injury, we gave TCV-116 (1 mg/kg per day PO), a nonpeptide Ang II type I receptor antagonist, or enalapril (10 mg/kg per day PO) to deoxycorticosterone acetate (DOCA)-salt hypertensive rats for 3 weeks and examined the effects on tissue mRNA levels for transforming growth factor-beta 1 (TGF-beta 1) and extracellular matrix components. Tissue mRNA levels were measured by Northern blot analysis. Renal mRNA levels for TGF-beta 1; types I, III, and IV collagen; and fibronectin in DOCA-salt hypertensive rats were increased by severalfold (P < .01) compared with sham-operated rats. In the aorta of DOCA-salt hypertensive rats, TGF-beta 1 and fibronectin mRNA levels were increased, but types I, III, and IV collagen mRNAs did not increase. In the heart, increased mRNA was found only for fibronectin. Thus, these gene expressions are regulated in a tissue-specific manner. TCV-116 or enalapril did not lower blood pressure in DOCA-salt hypertensive rats. However, the increase in renal mRNAs for TGF-beta 1 and extracellular matrix components in DOCA-salt hypertensive rats was significantly inhibited by treatment with TCV-116 or enalapril, which was associated with a significant decrease in urinary protein and albumin excretions and histological improvement of renal lesions. In contrast, in the aorta and heart these gene expressions were not affected by TCV-116 or enalapril. Thus, local Ang II may contribute to renal injury of DOCA-salt hypertension by stimulating the gene expression of TGF-beta 1 and extracellular matrix components.

Angiotensin II↗

PubMed1994

Prostaglandin E1 abrogates early reductive stress and zone-specific paradoxical oxidative injury in hypoperfused rat liver.

This study was designed to investigate the effects of prostaglandin E1 on reductive stress and the subsequent oxidative cell injury in hypoperfused rat liver. The intralobular heterogeneity of hepatocellular redox state, mitochondrial dysfunction, and intracellular hydroperoxide formation were visually monitored by digital microfluorography of pyridine nucleotide autofluorescence, rhodamine 123, and dichlorofluorescein fluorescence, respectively. Under the 25% low flow perfusion, pyridine nucleotide autofluorescence increased time-dependently and reached a steady state at 10 min among the entire lobules. The decrease in mitochondrial membrane potential was > 20 mV in all portions of the lobules at 60 min. The onset of hydroperoxide formation was observed at 40 min in the marginally oxygenated proximal portion of anoxic pericentral regions and the oxidative impact reached a maximum level at 60 min. Sodium (-)-8-(3-methoxy-4-phenylsulfinylphenyl) pyrazo [1,5-a]-1,3,5-triazine-4-olate monohydrate (BOF 4272), a novel xanthine oxidase inhibitor, suppressed the zone-specific oxidative changes without attenuating the increase in pyridine nucleotide autofluorescence and mitochondrial dysfunction. Pretreatment with prostaglandin E1 not only abrogated an early increase in pyridine nucleotide fluorescence and mitochondrial dysfunction induced by hypoperfusion but also diminished the subsequent midzonal oxidative injury. Since prostaglandin E1 has no oxyradical-scavenging action, the preventive effect of this reagent on the hypoxia-induced oxidative cell injury is attributable to the attenuation of mitochondrial dysfunction. These results suggest that, in low flow hypoxia, early reductive stress plays a key role in the initiation of xanthine oxidase-mediated midzonal oxidative changes, which may lead to subsequent centrilobular necrosis.

Alprostadil↗

PubMed1994

A novel cell layer without corticosteroid-synthesizing enzymes in rat adrenal cortex: histochemical detection and possible physiological role.

A stratum of cells that did not contain both aldosterone synthase cytochrome P450 (cytochrome P450aldo) and cytochrome P45011 beta was found immunohistochemically between the zona glomerulosa and the zona fasciculata of the rat adrenal cortex. As cytochromes P450aldo and P45011 beta are the enzymes responsible for the biosynthesis of aldosterone and corticosterone, respectively, the cells there are considered to be incapable of synthesizing both aldosterone and corticosterone. Furthermore, the cells are regarded as inert in producing adrenal androgens, because rat adrenal cortex is known to lack steroid 17 alpha-hydroxylase. Thus, the stratum is composed of cells that do not synthesize any of the major corticosteroids in significant quantities. It was 5-10 cells thick under normal feeding conditions, but diminished to 4-5 cells thick when animals were maintained under Na restriction, which is known to stimulate the secretion of angiotensin-II. When the distribution of 5-bromo-2'-deoxyuridine-labeled nuclei in the adrenocortex from BrdU-administered rats was examined, the stained nuclei were concentrated in and around the cell stratum. The pulse-chase experiments showed that the labeled cells migrated out of this layer and into the zonae fasciculata-reticularis. On the basis of these findings, we suggest that the newly discovered cell layer is the progenitor cell zone of the rat adrenal cortex.

Adrenal Cortex↗

PubMed1994

Stimulatory effect of pituitary adenylate cyclase-activating polypeptide on catecholamine synthesis in cultured bovine adrenal chromaffin cells: involvements of tyrosine hydroxylase phosphorylation caused by Ca2+ influx and cAMP.

In cultured bovine adrenal chromaffin cells, pituitary adenylate cylase-activating polypeptide (PACAP) stimulated [14C]catecholamine synthesis from [14C]tyrosine (but not from [14C]DOPA) in a concentration-dependent manner, causing maximal stimulation at 10(-7) M. The stimulatory action of PACAP was not affected by staurosporine (an inhibitor of protein kinase C) or in the cells in which protein kinase C was down-regulated by prolonged exposure to TPA (an activator of protein kinase C), whereas it was partially attenuated in Ca(2+)-free medium. PACAP (10(-7) M) increased the formation of [3H]inositol phosphates, [Ca2+]i and 45Ca2+ uptake as well as cAMP. The peptide also stimulated the phosphorylation of tyrosine hydroxylase, the enzyme catalyzing the rate-limiting step in catecholamine synthesis. Catecholamine synthesis and tyrosine hydroxylase phosphorylation stimulated by the maximal effective concentration of dibutyryl cAMP or high K+, which activates Ca2+ uptake, were further enhanced by PACAP, suggesting that both cAMP- and Ca(2+)-dependent protein kinases may be involved in the stimulation of tyrosine hydroxylase phosphorylation and catecholamine synthesis caused by PACAP.

Adrenal Medulla↗

PubMed1994

Steroid contents and cortical steroidogenic enzymes in non-hyperfunctioning adrenal adenoma.

The recent increasing use of ultrasound and computed tomography has revealed numbers of incidentally discovered adrenal tumors. Many studies have focused on their surgical management, but the biological characteristics of these adrenal tumors have remained unclear. Adrenal tumors were resected from 10 patients who underwent gastrectomy or cholecystectomy. No signs or symptoms of adrenal hormone excess or deficiency were evident either before or after the operation. Moreover, after surgery, no major differences in signs and symptoms including blood pressure levels were observed. Before surgery, neurogenic tumors and cysts were excluded by enhanced magnetic resonance imaging. Steroid contents and both the activities and amounts of steroidogenic cytochrome P-450s in the adrenocortical adenomas of these patients were examined. Microscopic examination revealed that the tumors were surrounded by a thin, non-intact capsule; the surrounding cortex was not atrophic and apparently normal; and the cells of both the tumor and adjacent portions were arranged in nests and cords. Measurements of all steroid content (pregnenolone, progesterone, corticosterone, 11-deoxycorticosterone, 18-hydroxydeoxycorticosterone, cortisol, and dehydroepiandrosterone) except aldosterone in 5 resected adrenal tumors were within the normal ranges for the adrenals of 5 patients with renal cell carcinoma. Aldosterone content in tumor portions was significantly lower than in the apparently normal adrenals. Although in both tumor and adjacent portions of another 5 resected adrenal tumors the activities and amounts of cytochrome P-450s (P-450scc, P-450(11 beta), P-450aldo, P-450(17 alpha), and P-450c21) were also within the normal ranges, the activities of P-450scc and P-450(17 alpha) in the tumor portion were greater than those in the adjacent portion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Neoplasms↗

PubMed1994

Renal protective effect of TCV-116 in stroke-prone spontaneously hypertensive rats.

We examined the effects of TCV-116, a non-peptide selective AT1 receptor antagonist, on cellular phenotype and on the expression of the transforming growth factor-beta 1 (TGF-beta 1) and extracellular matrix genes in the kidneys of stroke-prone spontaneously hypertensive rats (SHRSP). SHRSP were given vehicle or TCV-116 (10 mg/kg/day) by gastric gavage for 10 weeks (from the age of 22 to 32 weeks). Renal mRNA levels were measured by Northern blot analysis. In vehicle-treated 32-week-old SHRSP, urinary albumin excretion per 24 h was about 26-fold greater than that in age-matched Wistar-Kyoto (WKY) rats, and the mRNA levels of renal TGF-beta 1, fibronectin and collagen types I and III in SHRSP were all several-fold higher than those in WKY. Immunohistochemical studies showed the prominent presence of alpha-smooth muscle actin-expressing glomerular cells in SHRSP, in contrast to their absence in WKY. Treatment of SHRSP with TCV-116 decreased urinary albumin excretion and renal mRNA levels for TGF-beta 1 and for the above-mentioned extracellular matrix components. TCV-116 prevented the phenotypic modulation of glomerular cells in SHRSP. These results suggest that AT1 receptor antagonists may have powerful renal protective effects.

Albuminuria↗

PubMed1993

Essential role of the Arg112 residue of cytochrome P450cam for electron transfer from reduced putidaredoxin.

Cytochrome P450cam (CYP101) of Pseudomonas putida PpG1 in which Arg112 is substituted by Cys was isolated by in vitro random mutagenesis of the camC gene DNA coding for P450cam. The absorption spectra of the purified mutant enzyme were similar to those of the wild type enzyme, but its substrate-dependent NADH oxidation activity in the presence of putidaredoxin (Pd) and putidaredoxin reductase (PdR) was extremely low. The rate constant of electron transfer from reduced Pd to the heme of the mutant P450cam, measured on an anaerobic stopped flow apparatus, was 1/400 of that of the wild type enzyme and the dissociation constant of the mutant P450cam for oxidized Pd was several fold higher than that of the wild type enzyme. A considerable decrease in mid-point potential of the mutant enzyme was also noted. We conclude that Arg112, which is located on the surface of the P450cam molecule and hydrogen-bonded to one of the heme propionate chains, plays an essential role in the electron transfer from Pd.

Arginine↗

PubMed1993

Isolation and characterization of rat CYP11B genes involved in late steps of mineralo- and glucocorticoid syntheses.

We isolated and characterized four forms of rat CYP11B genes, which were tentatively named CYP11B1, -B2, -B3, and -B4. Genomic Southern analyses indicated that the members of the rat CYP11B gene subfamily were confined to these four genes; among them, CYP11B1 and -B2 encoded steroid 11 beta-hydroxylase and aldosterone synthase, respectively, while CYP11B3 was a gene highly homologous to CYP11B1 without a known expression product. By being devoid of a region spanning two exons conserved in the other three, CYP11B4 was presumably a pseudogene. In the nucleotide sequences, CYP11B1, -B3, and -B4 showed 95-96 and 93-100% identities in the coding and 0.5-kilobase 5'-flanking regions, respectively. However, the homology between the nucleotide sequences of one of the three and CYP11B2 was rather low, about 90 and 50% in the coding and 0.5-kilobase 5'-flanking regions, respectively. As a whole, CYP11B2 rather than CYP11B1, -B3, or -B4 was more homologous to CYP11B genes of other animals such as cow and human. In transient transfection experiments using mouse adrenocortical Y1 cells and chloramphenicol acetyltransferase gene constructs, the 0.5-kilobase 5'-flanking region of CYP11B1 had a 4- and 10-fold higher promoter activity than the corresponding regions of CYP11B2 and -B3, respectively. The possible presence of a suppressive element(s) was noted in the upstream of the 0.5-kilobase region of CYP11B1. Although a variant of cAMP-responsive element, which was present in rat CYP11B2 and all known CYP11B genes of other animals, was modified in rat CYP11B1 and -B3 genes, dibutyryl cAMP stimulated all the promoter activities of the 5'-flanking regions of the rat genes by 3-fold.

Amino Acid Sequence↗