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Loss of SIVA1 expression is associated with nasopharyngeal carcinoma.
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These findings collectively reveal a novel role for the p53 target gene SIVA both in regulating metabolism and in enabling tumorigenesis, independently of p53.
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Functional test demonstrated that Siva1 significantly inhibited the invasion and migration of HCT116 cells.
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electrical stimulation -inducible SIVA1 modulates p53 activities in proliferating keratinocytes, and exogenous electrical stimulation affects p53/HDM2/SIVA1 axis leading to increased proliferation during re-epithelialization
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SIVA1 interacts with RAD18 and serves as a molecular bridge between RAD18 and PCNA, thus targeting the E3 ligase activity of RAD18 onto PCNA.
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Siva1 promotes the ubiquitination and degradation of ARF, which in turn affects the stability of p53.
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Upon stimulation of thromboxane A2, degradation of Siva1 is impeded, resulting in an accumulation of the protein, which translocates from the nucleus to the cytosol.
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negative regulator of IL-2 gene expression in Treg cells
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Data show that low levels of Siva1 and Ser16-phosphorylated stathmin correlate with high metastatic states of breast cancer cells.
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These findings suggest that the caspase-dependent pathway for induction of apoptosis is involved in Siva-1-mediated influenza A virus replication.
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These results suggest that Siva-mediated unprovoked apoptosis is not likely to be involved in the pathogenesis of Familial Mediterranean fever.
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Siva-1 forms a functional complex with Tyk2 and participates in the transduction of signals that inhibit B lymphocyte growth.
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Siva-1 putative amphipathic helical region (SAH) binds BCL-XL and sensitizes cells to UV radiation induced apoptosis
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Overexpression of Siva-1 in T lymphocytes triggers the activation of a caspase-dependent death pathway including a pivotal mitochondrial step. Both N- and C-terminal domains of Siva proteins display the ability to induce a cell death process in T cells.
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Siva-1 has a role, through its inhibitory effect on NF-kappaB activity, in TCR-mediated AICD with implications in peripheral tolerance, T-cell homeostasis and cancer
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determined the N-terminal part of Siva as the binding region for CD27; the peroxisomal membrane protein PMP22 is a new interaction partner of Siva and may be involved in the host response against CVB3.
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Confirming the anti-apoptotic role of HPV-16 E7 in the HaCaT cellular model, evaluated by nuclear morphology, it was also found that Siva-1 expression produced a significant increase of the apoptotic rate in UV radiation-exposed HaCaT cells.
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Results suggest that Siva-1 might participate in the CD4-initiated signaling apoptotic pathway induced by the HIV-1 envelope in T-lymphoid cells.
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lysophosphatidic acid 2 receptor mediates down-regulation of Siva-1 to promote cell survival
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Data show that Siva and pyrin are co-expressed, and that pyrin modulates the apoptotic response to oxidative stress mediated by Siva.
