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It has been reported that induction of delta-9 desaturase activity is observed in situations characterized by an increased demand for unsaturated FA [40].
Recently, it has been reported that induction of mitochondrial apoptosis requires the involvement of the Bcl-2 family, including apoptosis inhibiting gene products (e.g., Bcl-2, Bcl-xL) and apoptosis accelerating gene products (e.g., Bax, Bak, Bcl-xS, Bim) [32].
It has been reported that induction of hepcidin is stimulated by IL-6 [ 19].
Recently, it has been reported that induction of EMT in differentiated immortalized human mammary epithelial cells led to the acquisition of the CD44+/CD24- stem-cell phenotype [ 41].
Previously, it has been reported that induction of MMP1 [ 18], MMP2 [ 19, 20] and MMP9 [ 21] expression were detected and correlated with poor prognosis in NPC due to the invasive and metastatic role of MMPs.
It has been reported that induction of experimental autoimmune encephalomyelitis (EAE) was blocked in mice deficient in either IL-17 or the Th17 polarizing cytokine IL-23, whereas mice deficient in either IFNγ or the Th1 polarizing cytokine IL-12 show increased susceptibility to EAE [ 50, 52, 53].
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Moreover, in CEACAMs-expressing mice colonized with AIEC bacteria, an increase of intestinal permeability has been reported that could be related to the induction of claudin-2 expression consequently to AIEC/CEACAM6 interaction [ 110].
Recently it has been reported that autophagy induction by SIRT6 through attenuation of insulin-like growth factor signaling is involved in human bronchial epithelial cell senescence (Takasaka et al., 2014).
Recently, it has been reported that the induction of EMT in differentiated immortalized human mammary epithelial cells led to the acquisition of the CD44+/CD24− stem cell phenotype [29].
It has also been reported that the induction of Mip-1α might coincide with the accumulation of N-acetylhexosaminyl glycoconjugates due to a Hexb deficiency in glial cells [31].
More recently, it has been reported that the induction of pluripotency in somatic cells can be achieved by the expression of defined transcription factors [2] [6], including either the combination of Oct4, Sox2, Klf4 and cMyc [2] [5], although the latter was found to be dispensable [7], or Oct4, Sox2, Nanog and Lin28 [6].
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