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Targeted disruption of the NF-IL6 gene discloses its essential role in bacteria killing and tumor cytotoxicity by macrophages

Article Abstract:

A study of the action of NF-IL6 in vivo through the development of NF-IL6(-/-) mice by gene targeting reveals its involvement in macrophage tumoricidal and bactericidal activities through an NO-independent mechanism. Activated macrophages from NF-IL6(-/-) mice that are prone to Listeria monocytogene infection release pathogens from the phagosome to the cytoplasm. Macrophages from NF-IL6(-/-) exhibit impaired tumor cytotoxicity. Both wild-type and NF-IL6(-/-) mice exhibit similar levels of NO formation.

Author: Akira, Shizuo, Tanaka, Takashi, Yoneda, Yoshihiro, Yoshida, Nobuaki, Suematsu, Sachiko, Yoshida, Kanji, Umemoto, Masanori, Shirafuji, Naoki, Fujiwara, Hiroshi, Kishimoto, Tadamitsu
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1995
Physiological aspects, Genetic aspects, Genetic engineering, Bacteriophages, Interleukin-6

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Calmodulin regulation of drosophila light-activated channels and receptor function mediates termination of the light response in vivo

Article Abstract:

Calmodulin (CAM) is involved in several intracellular transduction processes, responding to calcium changes. Studies of Dorsophila Cam mutants and the role of CAM in photorecptor cell function showed that transient phenotype of trp mutants is due to CAM regulation of the TRPL channel, and not by loss of store-operated conductance. CAM is shown to coordinate termintion of light responses through the modulation of receptor and ion channel activities.

Author: Zuker, Charles S., Scott, Kristin, Sun, Yumei, Beckingham, Kathy
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
Observations, Calmodulin

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Targeted overactivity of beta cell K(sub ATP) channels induces profound neonatal diabetes

Article Abstract:

A study in mice shows that decreased sensitivity of beta cell K(sub ATP) channels to ATP/ADP can cause diabetes. Increased ATP/ADP levels resulting from glucose metabolism stimulate the channel to close, which in turn triggers insulin secretion.

Author: Koster, J.C., Marshall, B.A., Ensor, N., Corbett, J.A., Nichols, C.G.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2000
Causes of, Diabetes, Diabetes mellitus, Potassium channels

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Subjects list: Research
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