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File: /var/www/html/application/controllers/Detail.php
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Severity: Warning
Message: Trying to access array offset on value of type null
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File: /var/www/html/application/models/Detail_model.php
File: /var/www/html/application/controllers/Detail.php
File: /var/www/html/index.php
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Filename: helpers/my_audit_helper.php
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Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
File: /var/www/html/application/controllers/Detail.php
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Filename: controllers/Detail.php
Line Number: 256
Backtrace:
File: /var/www/html/application/controllers/Detail.php
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File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
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File: /var/www/html/application/controllers/Detail.php
File: /var/www/html/application/controllers/Detail.php
File: /var/www/html/index.php
Positive feedback within a kinase signaling complex functions as a switch mechanism for NF-κB activation. | LitMetric
A switchlike response in nuclear factor-κB (NF-κB) activity implies the existence of a threshold in the NF-κB signaling module. We show that the CARD-containing MAGUK protein 1 (CARMA1, also called CARD11)-TAK1 (MAP3K7)-inhibitor of NF-κB (IκB) kinase-β (IKKβ) module is a switch mechanism for NF-κB activation in B cell receptor (BCR) signaling. Experimental and mathematical modeling analyses showed that IKK activity is regulated by positive feedback from IKKβ to TAK1, generating a steep dose response to BCR stimulation. Mutation of the scaffolding protein CARMA1 at serine-578, an IKKβ target, abrogated not only late TAK1 activity, but also the switchlike activation of NF-κB in single cells, suggesting that phosphorylation of this residue accounts for the feedback.
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