Parathyroid Hormone, Recombinant, Human (PTH) (1-84)

Polypeptide hormones secreted by the parathyroid glands, which promote release of calcium from bone to extracellular fluid by activating osteoblasts and inhibiting osteoclasts, indirectly promote increased intestinal absorption of calcium and promote renal tubular reabsorption of calcium and increased renal excretion of phosphates. It is a major regulator of bone metabolism. Secretion of parathyroid hormone increases when the level of calcium in the extracellular fluid is low. Its action is opposed by calcitonin. Parathyroid hormone (PTH), or parathormone, is secreted by the parathyroid glands as a polypeptide containing 84 amino acids. It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin (a hormone produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium concentration. PTH acts to increase the concentration of calcium in the blood by acting upon parathyroid hormone receptor in three parts of the body. PTH half-life is approximately 4 minutes. PTH enhances the release of calcium from the large reservoir contained in the bones. Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH. Stimulation is indirect since osteoclasts do not have a receptor for PTH; rather, PTH binds to osteoblasts, the cells responsible for creating bone. Binding stimulates osteoblasts to increase their expression of RANKL, which can bind to osteoclast precursors containing RANK, a receptor for RANKL. The binding of RANKL to RANK stimulates these precursors to fuse, forming new osteoclasts which ultimately enhances the resorption of bone.\n\nIn the kidney, PTH enhances active reabsorption of calcium and magnesium from distal tubules and the thick ascending limb. As bone is degraded both calcium and phosphate are released. It also greatly increases the excretion of phosphate, with a net loss in plasma phosphate concentration. By increasing the calcium:phosphate ratio more calcium is therefore free in the circulation. PTH enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. Vitamin D activation occurs in the kidney. PTH up-regulates 25-hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of calcium (as Ca2+ ions) by the intestine via calbindin. PTH was one of the first hormones to be shown to use the G-protein, adenylyl cyclase second messenger system. Normal total plasma calcium level ranges from 8.5 to 10.2mg/dL (2.12mmol/L to 2.55mmol/L).\n\nRecombinant human full length Parathyroid Hormone/1-84 is a single, non-glycosylated, polypeptide chain containing 84 amino acids. Has potential as an anti-osteoporotic agent due to its properties as a bone formation stimulant.\n\nAmino Acid Sequence: \nSVSEIQLMHN LGKHLNSMER VEWLRKKLQD VHNFVALGAP LAPRDAGSQR PRKKEDNVLV ESHEKSLGEA DKADVNVLTK AKSQ\n\nBiological Activity:\nRecombinant PTH is fully biologically active when compared to standards. The activity calculated by UMR106 cell/cAMP method corresponds to a specific activity of ~1x10e4 Units/mg.\n\nStorage and Stability:\nLyophilized powder may be stored at -20 degrees C. Stable for 12 months at -20 degrees C. Reconstitute with sterile ddH2O, 0.1% BSA or HSA. Aliquot to avoid repeated freezing and thawing. Store at -20 degrees C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

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SPECIFICATIONS

Catalog Number

P3109-28

Size

100ug

Form

Supplied as a lyophilized powder from 20mM PBS, pH 7.0, 50ug mannitol. Reconstitute with sterile ddH2O, 0.1% HSA or BSA to (same/more than)0.1mg/ml. Further dilution can be made with other aqueous solutions.

Purity

(same/more than)95% Purified by RP-HPLC and SDS-PAGE.

References

1. Seehofer, D., et al., Arch. Surg. 139(12): 1331-1338 (2004). 2. Maweja, S., et al., Arch. Surg. 139(12): 1301-1303 (2004). 3. Tebben, P.J., et al., Mayo Clin. Proc. 19(12): 1508-1513 (2004). 4. Fukata, S., et al., Arthritis Rheum. 50(12): 4060-4069 (2004). 5. Tominaga, Y., Clin. Calcium 14(1): 51-55 (2004). 6. Okuno, S., Clin. Calcium 14(1): 27-31 (2004).