|Other Names||Inhibin beta A chain, Activin beta-A chain, Erythroid differentiation protein, EDF, INHBA|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Inhibins and activins inhibit and activate, respectively, the secretion of follitropin by the pituitary gland. Inhibins/activins are involved in regulating a number of diverse functions such as hypothalamic and pituitary hormone secretion, gonadal hormone secretion, germ cell development and maturation, erythroid differentiation, insulin secretion, nerve cell survival, embryonic axial development or bone growth, depending on their subunit composition. Inhibins appear to oppose the functions of activins.|
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Provided below are standard protocols that you may find useful for product applications.
The inhibin beta A subunit joins the alpha subunit to forma pituitary FSH secretion inhibitor. Inhibin has been shown toregulate gonadal stromal cell proliferation negatively and to havetumor-suppressor activity. In addition, serum levels of inhibinhave been shown to reflect the size of granulosa-cell tumors andcan therefore be used as a marker for primary as well as recurrentdisease. Because expression in gonadal and various extragonadaltissues may vary severalfold in a tissue-specific fashion, it isproposed that inhibin may be both a growth/differentiation factorand a hormone. Furthermore, the beta A subunit forms a homodimer,activin A, and also joins with a beta B subunit to form aheterodimer, activin AB, both of which stimulate FSH secretion.Finally, it has been shown that the beta A subunit mRNA isidentical to the erythroid differentiation factor subunit mRNA andthat only one gene for this mRNA exists in the human genome.
Canzian, F., et al. Hum. Mol. Genet. 19(19):3873-3884(2010)Shi, F.T., et al. J. Clin. Endocrinol. Metab. 95 (10), E172-E180 (2010) :Lascorz, J., et al. Carcinogenesis 31(9):1612-1619(2010)Jugessur, A., et al. PLoS ONE 5 (7), E11493 (2010) :Johnatty, S.E., et al. PLoS Genet. 6 (7), E1001016 (2010) :
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