A Soluble C1b Protein and Its Regulation of Soluble Type 7 Adenylyl Cyclase†
نویسندگان
چکیده
منابع مشابه
A soluble C1b protein and its regulation of soluble type 7 adenylyl cyclase.
Adenylyl cyclase (AC) is a prototypical cell-signaling molecule expressed in virtually all organisms from bacteria to man. While C1b, a poorly conserved region within mammalian AC, has been implicated in numerous isoform-specific regulatory properties, no one has purified the C1b region as a functional protein to homogeneity in order to study its role in enzyme function. We hypothesize that C1b...
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Soluble adenylyl cyclase (sAC) represents a novel form of mammalian adenylyl cyclase structurally, molecularly, and biochemically distinct from the G protein-regulated, transmembrane adenylyl cyclases (tmACs). sAC possesses no transmembrane domains and is insensitive to classic modulators of tmACs, such as heterotrimeric G proteins and P site ligands. Thus, sAC defines an independently regulate...
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Mammalian membrane-bound adenylyl cyclase consists of two highly conserved cytoplasmic domains (C1a and C2a) separated by a less conserved connecting region, C1b, and one of two transmembrane domains, M2. The C1a and C2a domains form a catalytic core that can be stimulated by forskolin and the stimulatory G protein subunit alpha (Galpha(s)). In this study, we analyzed the regulation of type 7 a...
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Soluble adenylyl cyclase (sAC) is a recently identified source of the ubiquitous second messenger cyclic adenosine 3',5' monophosphate (cAMP). sAC is distinct from the more widely studied source of cAMP, the transmembrane adenylyl cyclases (tmACs); its activity is uniquely regulated by bicarbonate anions, and it is distributed throughout the cytoplasm and in cellular organelles. Due to its uniq...
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of a dissertation at the University of Miami. Retinal ganglion cells (RGCs) as well as other CNS neurons do not regenerate after injury and die soon after. While significant progress has been made in understanding the molecular basis for this lack of regenerative ability, this knowledge has not been enough to generate effective therapeutic strategies to promote axonal regeneration or prevent ce...
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ژورنال
عنوان ژورنال: Biochemistry
سال: 2004
ISSN: 0006-2960,1520-4995
DOI: 10.1021/bi049088+