Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.5.3.1 extracted from

  • Niese, K.; Collier, A.; Hajek, A.; Cederbaum, S.; OBrien, W.; Wills-Karp, M.; Rothenberg, M.; Zimmermann, N.
    Bone marrow cell derived arginase I is the major source of allergen-induced lung arginase but is not required for airway hyperresponsiveness, remodeling and lung inflammatory responses in mice (2009), BMC Immunol., 10, 33.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine bone marrow cell derived arginase I is the predominant source of allergen-induced lung arginase but is not required for allergen-induced inflammation, airway hyperresponsiveness or collagen deposition Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining

General Information

General Information Comment Organism
physiological function in arginase I-deficient bone marrow chimeric mice, following transfer of arginase I-deficient bone marrow into irradiated recipient mice, arginase I expression is not required for hematopoietic reconstitution and baseline immunity. Arginase I deficiency in bone marrow-derived cells decreases allergen-induced lung arginase by 85.8%. Arginase II-deficient mice have increased lung arginase activity following allergen challenge to a similar level to wild type mice. Bone-marrow-derived arginase I is not required for allergen-elicited sensitization, recruitment of inflammatory cells in the lung, and proliferation of cells. Allergen-induced airway hyperresponsiveness and collagen deposition are similar in arginase-deficient and wild type mice. Arginase II-deficient mice respond similarly to their control wild type mice with allergen-induced inflammation, airway hyperresponsiveness, proliferation and collagen deposition Mus musculus