Disease relevance of Cinda1

• Understanding the action of genetic factors, such as Cinda1 and Cinda2, that control T cell function is expected to contribute to the efficient analysis of the genetic control of susceptibility to infections and autoimmune diseases [1].
• Thus the present study shows that S-methyl-L-thiocitrulline can potently block cytokine induced activation of nitric oxide synthase in pancreatic islets, but using the presently adopted administration protocol failed to protect against development of insulin-dependent diabetes mellitus in vivo [2].

High impact information on Cinda1

• In vitro evidence suggests that cytokine-induced activation of the transcription factor NF-kappaB is an important component of the signal triggering beta cell apoptosis [3].
• Cytokine-induced activation of nuclear factor-kappa B is inhibited by hydrogen peroxide through oxidative inactivation of IkappaB kinase [4].
• The cytokine-induced activation of Rac was augmented in a 32D/EpoR-Wt clone that inducibly overexpresses the adaptor protein CrkL or the Ras guanine nucleotide exchange factor C3G, which forms a complex with CrkL [5].
• Cytokine-induced activation of glial cells in the mouse brain is enhanced at an advanced age [6].
• Interestingly, cytokine-induced activation of both astrocytes and microglia was significantly more marked in the brain of aged animals, in which it included numerous ameboid microglia, than of younger age groups [6].

Biological context of Cinda1

• To map some of these genes, we tested F2 hybrids between one of the high-responder RC strains, CcS-4, and the low-responder parental strain BALB/c. We found that the response to high IL-2 concentrations is controlled by a locus, Cinda1 (cytokine-induced activation 1), on chromosome 11 near the marker D11Mit4 [1].
• Electromobility shift and luciferase reporter gene assays permitted the analysis of cytokine-induced activation of the NF-kappaB pathway [7].

Anatomical context of Cinda1

• It may be that IL-2 and IFN-alpha are often not sufficiently effective because intratumoral monocytes/macrophages (MO) inhibit the cytokine-induced activation of cytotoxic effector lymphocytes such as NK-cells at the site of tumor growth [8].
• Cytokine-induced activation of signal transducer and activator of transcription in photoreceptor precursors regulates rod differentiation in the developing mouse retina [9].

Associations of Cinda1 with chemical compounds

• The cytokine-induced activation of caspase-3 and LDH-release was inhibited by estradiol in estrogen receptor-independent way [10].

Other interactions of Cinda1

• Glycosphingolipid synthesis inhibitor represses cytokine-induced activation of the Ras-MAPK pathway in embryonic neural precursor cells [11].
• In the latter instance the signals triggering cytokine production are crucial since IL-10 interferes with bacterial but not viral or cytokine-induced activation of expression of cytokine genes [12].

Analytical, diagnostic and therapeutic context of Cinda1

• In electrophoretic mobility shift assays, oxidized EPA but not unoxidized EPA potently inhibited cytokine-induced activation of endothelial nuclear factor-kappaB (NF-kappaB) [13].

References