Differential distribution of cytochrome P-450 and cytochrome P-448 in liver microsomal membranes

Glaumann, Hans; Kuylenstierna, Bo; Dallner, Gustav

doi:10.1016/0024-3205(69)90187-8

Cited by 12 publications

(1 citation statement)

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“…After PAH treatment of rats, a second form of liver microsomal cytochrome P-450, called “P-448” could be detected spectrophotometrically (Glaumann et al , 1969; Lu et al , 1971); another lab termed the PAH-inducible enzyme “P 1 -450” (Parli and Mannering, 1970). It was thus postulated that “AHH activity” was “P-448” or “P 1 -450.” Therefore, a spectrophotometric assay — to study the height and location of the Soret peak — was carried out in PAH-treated fetal hamster cell cultures; indeed, upon treatment of the cell homogenate with NADPH and CO, a peak developed and was associated with increasing AHH activity as a function of time, during which the Soret peak shifted from 450 to 446 nm (Nebert, 1970).…”

Section: History and Backgroundmentioning

confidence: 99%

Aryl hydrocarbon receptor (AHR): “pioneer member” of the basic-helix/loop/helix per - Arnt - sim (bHLH/PAS) family of “sensors” of foreign and endogenous signals

Nebert

2017

Progress in Lipid Research

201

177

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The basic-helix-loop-helix Per-Arnt-Sim (bHLH/PAS) family comprises many transcription factors, found throughout all three kingdoms of life; bHLH/PAS members “sense” innumerable intracellular and extracellular “signals” — including endogenous compounds, foreign chemicals, gas molecules, redox potential, photons (light), gravity, heat, and osmotic pressure. These signals then initiate downstream signaling pathways involved in responding to that signal. The term “PAS”, abbreviation for “Per-Arnt-Sim” was first coined in 1991. Although the mouse Arnt gene was not identified until 1991, evidence of its co-transcriptional binding partner, aryl hydrocarbon receptor (AHR), was first reported in 1974 as a “sensor” of foreign chemicals, up-regulating cytochrome P450 family 1 (CYP1) and other enzyme activities that usually metabolize the signaling chemical. Within a few years, AHR was proposed also to participate in inflammation. The mouse [Ah] locus was shown (1973–1989) to be relevant to chemical carcinogenesis, mutagenesis, toxicity and teratogenesis, the mouse Ahr gene was cloned in 1992, and the first Ahr(−/−) knockout mouse line was reported in 1995. After thousands of studies from the early 1970s to present day, we now realize that AHR participates in dozens of signaling pathways involved in critical-life processes, affecting virtually every organ and cell-type in the animal, including many invertebrates.

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Section: History and Backgroundmentioning

confidence: 99%