Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Acts as an anti-apoptotic factor and its absence increases cell death under normal and stress conditions.
Showing 10 out of 13 products:
these findings indicate that the stability of the DDIAS protein is regulated by CHIP/HSP70 (Montrer HSP70 Anticorps)-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 (Montrer CCND1 Anticorps) and Cyclin E1 (Montrer CCNE1 Anticorps) through activating P38 (Montrer CRK Anticorps)-activating transcription factor 2 (Montrer ATF2 Anticorps) signaling pathway, thus enhanced cell growth of breast cancer
EGF (Montrer EGF Anticorps) activates the ERK5 (Montrer MAPK7 Anticorps)/MEF2 (Montrer MEF2A Anticorps) pathway, which in turn induces DDIAS expression to promote cancer cell invasion by activating beta-catenin (Montrer CTNNB1 Anticorps) target genes
DDIAS is a target of NFATc1 (Montrer NFATC1 Anticorps) and is associated with cisplatin resistance in lung cancer cells.
NOXIN overexpression, as a result of genomic DNA gain or amplification, promotes HCC (Montrer FAM126A Anticorps) tumorigenesis by accelerating DNA synthesis and cell cycle progression, where NOXIN functions as a cofactor of DNA polymerase (Montrer POLB Anticorps)-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