Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.7.49 (
reverse transcriptase
)
31,746
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Human hepatic stimulator substance (hHSS) is a newly identified growth-promoting factor in liver.
HSS
is capable of stimulating the hepatic regeneration in hepaectomized rats and promoting the growth of hepatic tumor cells. To understand and elucidate the regulation of hHSS on hepatocyte growth at genetic level, the 4,890 bp of 5'-flanking region of hHSS gene have been isolated and sequenced. On basis of comparison of the 5'-flanking sequences with GenBank, hHSS gene was localized on human chromosome 16. Transcriptional start site was identified by
reverse transcriptase
-polymerase chain reaction (RT-PCR) and 5' rapid amplification of cDNA end (5'RACE). The initiation nucleotide was defined as 'C', which located at 254 bp upstream of the reported sequence of exon I.
...
PMID:[Cloning and structural analysis of 5'-flanking sequence of human hepatic stimulator substance (hHSS) gene]. 1498 37
The bisphosphonate class of antiresorptive drugs and active forms of parathyroid hormone (PTH (1-34)) have been used clinically to enhance bone mass and density in patients with osteoporosis. Abundant evidence suggests that the mechanism by which PTH (1-34) increases bone density is stimulation of osteoblast differentiation. Although bisphosphonates have been classically thought to increase bone density by inhibiting osteoclasts, there is increasing evidence to suggest that bisphosphonates have direct stimulatory effects on osteoblast differentiation. Interestingly, in patients with osteoporosis, combination therapy with bisphosphonates and PTH (1-34) is not synergistic in increasing bone density; bisphosphonates appear to blunt the effect of PTH (1-34). To begin to understand the mechanism governing the effects of these agents on osteoblasts and a possible explanation for their apparent antagonism, we examined the expression of several bone morphogenetic proteins (BMPs) in MC3T3-E1 preosteoblastic cells either untreated, or treated with alendronate, parathyroid hormone, or a combination of the two agents. We find by
reverse transcriptase
-polymerase chain reaction (RT-PCR) that while alendronate fails to induce the expression of any of the BMPs tested, several BMPs are induced by PTH (1-34). The induction of the PTH (1-34)-inducible BMPs is blocked with simultaneous alendronate treatment. These data suggest that alendronate interferes with PTH (1-34)-induced BMP gene transcription and provides a possible basis for the antagonism observed between the two agents in increasing bone density.
HSS
J 2007 Sep
PMID:Alendronate inhibits PTH (1-34)-induced bone morphogenetic protein expression in MC3T3-E1 preosteoblastic cells. 1875 89