-
Results show that abolishing ICP0:SIAH-1 interaction affects the HSV-2 phenotype during infection. In vitro, the SIAH-binding deficient mutant synthesized significantly less DNA and protein, and virus growth was clearly attenuated compared to wild-type virus. In model mice, HSV-2 carrying the SIAH-binding deficient mutation caused an acute infection in the murine eye and was able to spread to the innervating neurons.
-
Using the novel PUM1 and PUM2 mRNA target SIAH1 as a model, this study shows mechanistic differences between PUM1 and PUM2 and between NANOS1, 2, and 3 paralogues in the regulation of SIAH1.
-
Depletion of KDM3A coincided with the loss of SIAH1 induction and the accumulation of dimethylated H3K9 surrounding the SIAH1 promoter. Interestingly, KDM3A expression was also up-regulated by nutritional stress in a HIF-1alpha dependent manner.
-
The crystallographic models provide structural insights into the substrate binding of the SIAH family E3 ubiquitin ligases that are critically involved in regulating cancer-related pathways.
-
Results showed that SIAH1 and PTP4A1 expression was regulated by mir-944 in breast cancer cells. miR-944 binds directly the 3 UTR of their promotor region.
-
Study identified SIAH1/2 (SIAH) as the E3 ligase mediating Wnt-induced Axin degradation. SIAH proteins promote the ubiquitination and proteasomal degradation of Axin through interacting with a VxP motif in the GSK3-binding domain of Axin, and this function of SIAH is counteracted by GSK3 binding to Axin.
-
results suggest that CacyBP/SIP is involved in regulation of the Hsp90 chaperone machinery
-
PINK1 disease mutants failed to recruit synphilin-1 and did not activate mitophagy, indicating that PINK1-synphilin-1-SIAH-1 represents a new parkin-independent mitophagy pathway. Drugs that activate this pathway will provide a novel strategy to promote the clearance of damaged mitochondria in Parkinson's disease.
-
Results suggest that activated STAT3 regulates active beta-catenin protein levels via stabilization of SIAH-1 and the subsequent ubiquitin-dependent proteasomal degradation of beta-catenin in HEK293T cells.
-
Siah-1 expression was observed in 41.4% of oral squamous cell carcinoma. Siah-1 was expressed in the cytoplasm and cell membranes, and partially in the nucleus .
-
SIAH1 is associated with a tumor promoting role in breast cancer.
-
In neuroblastoma cells, siRNA silencing of SIAH1 promoted cellular proliferation and suppressed apoptosis. Protein and mRNA expression of alpha-synuclein, LC3-II and p53 decreased after SIAH1 knockdown. E1 protein and mRNA levels increased after SIAH1 siRNA.
-
Results demonstrated that miR-107 directly down-regulated SIAH1 expression in human breast cancer cells. An inverse correlation between the expression of miR-107 and SIAH1 was found in human breast cancer tissues and cell lines.
-
Similar to TAp73, DNp73 is stabilized by hypoxia in a HIF-1a-dependent manner, which otherwise is degraded by Siah1.
-
findings demonstrate that dissociation of the GAPDH/Siah1 pro-apoptotic complex can block high glucose-induced pericyte apoptosis, widely considered a hallmark feature of DR
-
Data indicate that ubiquitin ligase Siah as a regulator of to Mesenchymal Transition (EMT) by controlling the abundance of the key transcription factor Zeb1, while Siah itself is subject to regulation by EMT-inducing factors.
-
miRNA network regulates SIAH1 in in colorectal metastasis tissues.
-
CDK2 up-regulates the protein level of KLF10 through reducing its association with SIAH1, a KLF10 E3-ubiqutin ligase involved in proteasomal degradation.
-
molecular basis of Siah1 and Siah2 E3 ubiquitin ligase substrate specificity
-
Siah1 is a substrate of ASK1 for activation of the GAPDH-Siah1 oxidative stress signaling cascade.
