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Acts as an anti-apoptotic factor and its absence increases cell death under normal and stress conditions.
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these findings indicate that the stability of the DDIAS protein is regulated by CHIP/HSP70 (show HSP70 Antibodies)-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 (show CCND1 Antibodies) and Cyclin E1 (show CCNE1 Antibodies) through activating P38 (show CRK Antibodies)-activating transcription factor 2 (show ATF2 Antibodies) signaling pathway, thus enhanced cell growth of breast cancer
EGF (show EGF Antibodies) activates the ERK5 (show MAPK7 Antibodies)/MEF2 (show MEF2A Antibodies) pathway, which in turn induces DDIAS expression to promote cancer cell invasion by activating beta-catenin (show CTNNB1 Antibodies) target genes
DDIAS is a target of NFATc1 (show NFATC1 Antibodies) and is associated with cisplatin resistance in lung cancer cells.
NOXIN overexpression, as a result of genomic DNA gain or amplification, promotes HCC (show FAM126A Antibodies) tumorigenesis by accelerating DNA synthesis and cell cycle progression, where NOXIN functions as a cofactor of DNA polymerase (show POLB Antibodies)-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