Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.69 (BMT)
2,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously reported on the purification of a serum calcium-decreasing factor, referred to as caldecrin, from porcine pancreas, that is thought to be a serine protease (Tomomura, A., Fukushige, T., Noda, T., Noikura, T., and Saheki, T. (1992) FEBS Lett. 301, 277-281). In the present study, we purified caldecrin from rat pancreas and determined its primary structure by cDNA cloning. The predicted caldecrin protein is presumed to be synthesized as a preproenzyme of 268 amino acids with a signal peptide of 16 amino acids and an activation peptide of 13 amino acids, and is, with the exception of a central region, almost identical to the reported rat pancreatic elastase IV sequence. The caldecrin gene is selectively expressed in the pancreas, as judged by Northern blot analysis. After expression in BMT-10 cells, immunoreactive caldecrin was found in the culture supernatant, and it inhibited the parathyroid hormone-stimulated 45Ca release from cultured fetal long bones. Catalytic site mutants were synthesized in a baculovirus system, and recombinant mutants also decreased the serum calcium level of mice. These data implicate caldecrin, a protease closely related to elastase IV, in the regulation of blood calcium levels.
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PMID:Molecular cloning and expression of serum calcium-decreasing factor (caldecrin). 853 Apr 54

Post-BMT subjects have an increased bone fracture risk. Additionally, several factors were associated with osteopenia and osteoporosis in these individuals. We aimed to identify other factors associated with osteopenia and osteoporosis in allogeneic post-BMT subjects. We conducted a cross-sectional study with 47 allogeneic post- BMT subjects. Serum 25-hydroxyvitamin D (25(OH)D), parathyroid hormone, ferritin, vitamin B(12), insulin, glucose, cholesterol and triglyceride levels were measured. Insulin resistance and secretion were estimated through the homeostatic model assessment for insulin resistance (HOMA-IR) and homeostatic model assessment for beta-cell function (HOMA-B), respectively. A bone densitometry (BMD) was also obtained. The median time after BMT was 47.7 (12-115) months. Osteoporosis was identified in 17.0% of the subjects and osteopenia in 19.7%. The mean serum ferritin (P=0.002), insulin (P<0.0001), glucose (P=0.003) and triglyceride (P=0.018) levels were higher in individuals with osteopenia/osteoporosis. HOMA-IR (P<0.0001) and HOMA-B (P<0.0001) were increased in post-BMT subjects with osteopenia/osteoporosis. There was no other factor associated with the outcome. After adjustments ferritin, serum 25(OH)D and HOMA-IR remained independently associated with osteopenia/osteoporosis; however triglycerides no longer were. In conclusion, in the present study, low serum 25(OH)D levels, high serum ferritin levels and insulin resistance were associated with osteopenia/osteoporosis in post-BMT subjects.
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PMID:Low bone mineral density is associated with insulin resistance in bone marrow transplant subjects. 1936 30

Transplantation of whole bone marrow (BMT) leads to engraftment of both osteoprogenitor cells and hematopoietic cells; however, the robust osteopoietic chimerism seen early after BMT decreases with time. Using our established murine model, we demonstrate that a post-BMT regimen of either granulocyte-colony stimulating factor, growth hormone, parathyroid hormone, or stem cell factor each stimulates greater donor osteoblast chimerism at 4 months posttransplantation than saline-treated controls and approximates the robust osteopoietic chimerism seen early after BMT; however, only growth hormone led to significantly more donor-derived osteocytes than controls. Importantly, there were no adverse hematologic consequences of the different treatments. Our data demonstrate that these cytokines can stimulate the differentiation of transplanted donor marrow cells into the osteopoietic lineage after BMT. Post-BMT cytokine therapy may generate durable osteopoietic engraftment, which should lead to sustained clinical benefit and render BMT more applicable to bone disorders.
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PMID:Cytokine-induced osteopoietic differentiation of transplanted marrow cells. 2171 5