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G Proteins, Receptors, and Disease (Hardcover, 1998 ed.)
Loot Price: R6,168
Discovery Miles 61 680
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G Proteins, Receptors, and Disease (Hardcover, 1998 ed.)
Series: Contemporary Endocrinology, 6
Expected to ship within 10 - 15 working days
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"Theoretically, one should obtain essentially the same clinical
picture from failure of an end-organ to respond to a hormone as
from a decreased production or absence of said hormone. " With
these words, Fuller Albright began his now classic paper describing
a novel disease, pseudo hypoparathyroidism (PHP), and a novel
concept, hormone resis- tance as a cause of disease. Soon, other
hormone resistance disorders such as nephrogenic diabetes insipidus
(NDI) were recognized, and the concept was extended to resistance
to other substances such as calcium ions in familial hypocalciuric
hypercalcemia (FHH). Later, diseases characterized by excess rather
than deficient hormone action such as McCune-Albright syndrome
(MAS) and familial male precocious puberty (FMPP) were recognized
to be caused by autonomous endocrine hyperfunction. Although many
i!!vestigators provided careful and detailed descriptions of the
clinical features of these and other related endocrine disorders,
an understanding of pathogenesis proved elusive for many years. In
just the past few years, we have gone from clinical description to
a molecular understanding of these interesting disorders. This
remarkable progress reflects a synthe- sis of three distinct, but
now overlapping, areas of biomedical research: the aforemen- tioned
recognition and careful clinical description of specific diseases,
the elucidation of the basic mechanisms of signal transduction, and
the application of the powerful tools of molecular biology and
genetics. Fundamental studies on the mechanisms of hormone action
by Rodbell and colleagues at NIH culminated in the discovery of a
major signal transduction pathway involving heterotrimeric G
proteins.
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