IL-12-dependent activation of ERK1/2 in human T lymphoblasts

Canda-Sánchez, Ana; Salgado, Francisco; Pérez-Díaz, Amparo; Varela-González, Carla; Arias, Pilar; Nogueira, Marco Aurélio

doi:10.1016/j.imbio.2008.07.006

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…To block the reaction, an equal volume of FBS was added and cells were thoroughly washed before counting. Initial cell density was 50,000 cells/well (0.25 × 10 6 PBMC/ml; 96‐round bottom well microplates), and 2 μg/ml PHA was used as mitogen (34). Each experimental condition was tested nine times.…”

Section: Methodsmentioning

confidence: 99%

CD26: A negative selection marker for human Treg cells

et al. 2012

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Section: Methodsmentioning

confidence: 99%

CD26: A negative selection marker for human Treg cells

et al. 2012

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Upregulation of nuclear factor-κB expression by SLURP-1 is mediated by α₇-nicotinic acetylcholine receptor and involves both ionic events and activation of protein kinases

Chernyavsky

Arredondo

Galitovskiy

et al. 2010

American Journal of Physiology-Cell Physiology

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SLURP-1 (secreted mammalian Ly-6/urokinase plasminogen activator receptor-related protein-1) is a novel auto/paracrine cholinergic peptide that can bind to α(7)-nicotinic acetylcholine receptor (nAChR), a high Ca(2+)-permeable ion channel coupled to regulation of nuclear factor-κB (NF-κB) expression. Elucidation of intracellular signaling events elicited by SLURP-1 is crucial for understanding the molecular mechanism of functioning of this novel hormone-like peptide that alters vital cell functions and can protect from tumorigenic transformation. In this study, we sought to dissect out the role of α(7)-nAChR in mediating the biologic effects of recombinant SLURP-1 on the immortalized line of human oral keratinocytes Het-1A. A multifold upregulation of the NF-κB expression at the mRNA and protein levels by SLURP-1 was only slightly diminished due to elimination of Na(+), whereas in Ca(2+)-free medium the effect of SLURP-1 was inhibited by >50%. Both in the absence of extracellular Ca(2+) and in the presence of Cd(2+) or Zn(2+), the SLURP-1-dependent elevation of NF-κB was almost completely blocked by inhibiting MEK1 activity. Downstream of α(7)-nAChR, the SLURP-1 signaling coupled to upregulation of NF-κB also involved Jak2 as well as Ca(2+)/calmodulin-dependent kinase II (CaMKII) and protein kinase C (PKC), whose inhibition significantly (P < 0.05) reduced the SLURP-1-induced upregulation of NF-κB. The obtained results indicated that activation of α(7)-nAChR by SLURP-1 leads to upregulation of the NF-κB gene expression due to activation of the Raf-1/MEK1/ERK1/2 cascade that proceeds via two complementary signaling pathways. One is mediated by the Ca(2+)-entry dependent CaMKII/PKC activation and another one by Ca(2+)-independent involvement of Jak2. Thus, there exists a previously not appreciated network of noncanonical auto/paracrine ligands of nAChR of the Ly-6 protein family, which merits further investigations.

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IL-12-dependent activation of ERK1/2 in human T lymphoblasts

Cited by 2 publications

References 21 publications

CD26: A negative selection marker for human Treg cells

CD26: A negative selection marker for human Treg cells

Upregulation of nuclear factor-κB expression by SLURP-1 is mediated by α₇-nicotinic acetylcholine receptor and involves both ionic events and activation of protein kinases

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IL-12-dependent activation of ERK1/2 in human T lymphoblasts

Cited by 2 publications

References 21 publications

CD26: A negative selection marker for human Treg cells

CD26: A negative selection marker for human Treg cells

Upregulation of nuclear factor-κB expression by SLURP-1 is mediated by α7-nicotinic acetylcholine receptor and involves both ionic events and activation of protein kinases

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Upregulation of nuclear factor-κB expression by SLURP-1 is mediated by α₇-nicotinic acetylcholine receptor and involves both ionic events and activation of protein kinases