Instructions: Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
Input: To examine the effect of TRIB3 on endoplasmic reticulum stress induced -cell apoptosis and to investigate the mechanism with a specific emphasis on the role of NF-B pathway.', 'We investigated the effect of TRIB3 on ER stress-induced -cell apoptosis in INS-1 cells and primary rodent islets. The potential role of TRIB3 in ER stress inducer thapsigargin (Tg)-induced -cell apoptosis was assessed using overexpression and siRNA knockdown approaches. Inducible TRIB3 -cells, regulated by the tet-on system, were used for sub-renal capsule transplantation in streptozotocin (STZ)-diabetic mice, to study the effect of TRIB3 on ER stress-induced -cell apoptosis in vivo. Apoptosis was determined by TUNEL staining both in vivo and in vitro, while the molecular mechanisms of NF-B activation were investigated.', 'TRIB3 was induced in ER-stressed INS-1 cells and rodent islets, and its overexpression was accompanied by increased -cell apoptosis. Specifically, TRIB3 overexpression enhanced Tg-induced INS-1 derived -cell apoptosis both in vitro and in sub-renal capsular transplantation animal model. Additionally, knockdown of Trib3 blocked Tg-induced apoptosis. Mechanistically, the induction of TRIB3 during ER stress resulted in the activation of NF-B and aggravated INS-1 derived -cell apoptosis, while inhibiting the NF-B pathway significantly abrogated this response and prevented -cell apoptosis, both in vitro and in sub-renal capsular transplantation animal model.
Output:
Does tRIB3 alter endoplasmic reticulum stress-induced -cell apoptosis via the NF-B pathway?