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Acts as an anti-apoptotic factor and its absence increases cell death under normal and stress conditions. Additionally we are shipping C11orf82 Antibodies (16) and C11orf82 Proteins (4) and many more products for this protein.
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these findings indicate that the stability of the DDIAS protein is regulated by CHIP/HSP70-mediated proteasomal degradation and that CHIP overexpression stimulates the apoptosis of lung cancer cells in response to DNA-damaging agents
Noxin facilitated the expression of Cyclin D1 and Cyclin E1 through activating P38-activating transcription factor 2 signaling pathway, thus enhanced cell growth of breast cancer
EGF activates the ERK5/MEF2 pathway, which in turn induces DDIAS expression to promote cancer cell invasion by activating beta-catenin target genes
DDIAS is a target of NFATc1 and is associated with cisplatin resistance in lung cancer cells.
NOXIN overexpression, as a result of genomic DNA gain or amplification, promotes HCC tumorigenesis by accelerating DNA synthesis and cell cycle progression, where NOXIN functions as a cofactor of DNA polymerase-primase complex
Noxin may be a component of the cell defense system: it is activated by various stress stimuli, helps cells to withdraw from cycling, and opposes apoptosis.
Acts as an anti-apoptotic factor and its absence increases cell death under normal and stress conditions. Can induce cell cycle arrest in the G1 or early S phase and this activity is independent of p53/TP53 (By similarity).
nitric oxide-inducible gene protein