Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.2.3.23 (GAS)
 957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

PC12 cells were used to compare signaling pathways activated by alpha1-adrenergic receptor (AR) subtypes. PC12 cells were transfected with human alpha1A, alpha1B, or alpha1D-ARs, and subclones stably expressing receptor densities in physiological ranges isolated and characterized. Norepinephrine (NE) activated a large number of signaling pathways in transfected cells, including inositol phosphate formation, intracellular calcium, all three arms of the mitogen activated protein kinase pathways, and a number of tyrosine kinases. Activation of mitogen activated protein kinase pathways and tyrosine kinases was not blocked by chelation of intracellular calcium with BAPTA or inhibition of protein kinase C. NE also activated luciferase reporter constructs for seven different transcription factors (AP1, SRE, CRE, NFkappaB, NFAT, Stat, GAS) following transfection into alpha1A-AR expressing PC12 cells. However, similar increases in inositol phosphate formation and intracellular Ca2+ caused by purinergic P2Y2 receptor activation did not activate any of these reporters. Comparison of alpha1-AR subtypes showed that the alpha1A activated all seven reporters, the alpha1B showed smaller effects, while the alpha1D was ineffective. NE caused differentiation of alpha1A, but not alpha1B or alpha1D, -AR expressing PC12 cells similar to that caused by NGF. This NE-induced differentiation was reduced or blocked by all inhibitors tested. We conclude that alpha1-ARs activate many signaling pathways and transcriptional responses in PC12 cells, which are not linearly related to second messenger production, and which may differ for different alpha1-AR subtypes.
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PMID:Signaling pathways activated by alpha1-adrenergic receptor subtypes in PC12 cells. 1135 36

Group A streptococcus (GAS, Streptococcus pyogenes), group B streptococcus (GBS, Streptococcus agalactiae) and pneumococcus (Streptococcus pneumoniae) are all human pathogens that cause significant morbidity and mortality worldwide. These related species cause different spectra of infections spanning from trivial upper respiratory tract or skin infections to septic and severe diseases. In order to cause deep infections and survive in the human body the bacteria must evade the immune system. Complement is an important part of innate immunity both as an opsonizing and membrane destructing cascade and as an effector system of antibodies. In this review, we describe the complement resistance mechanisms of the three clinically most important streptococcal species, groups A and B streptococci and pneumococcus. The complement evasion mechanisms of these three species are analogous, yet different from one another. Several strains of all three species express molecules (M-proteins, Bac or beta, PspC) that acquire host fluid-phase complement regulators factor H or C4b binding protein to their surfaces. Groups A and B streptococci also secrete proteins and/or enzymes that inhibit the activation of the complement system or chemotaxis caused by the complement activation products. Even though a lot is known about the immune evasion by streptococci, the high morbidity and mortality associated with infections caused by streptococci and the need for efficient vaccines warrant further studies on the streptococcal molecules mediating complement resistance.
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PMID:Complement resistance mechanisms of streptococci. 1291 16