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anti-Human Apoptosis Inhibitor 5 Antibodies:
anti-Mouse (Murine) Apoptosis Inhibitor 5 Antibodies:
anti-Rat (Rattus) Apoptosis Inhibitor 5 Antibodies:
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Human Monoclonal Apoptosis Inhibitor 5 Primary Antibody for IF, IHC (p) - ABIN521982
Garcia-Jove Navarro, Basset, Arcondéguy, Touriol, Perez, Prats, Lacazette: Api5 contributes to E2F1 control of the G1/S cell cycle phase transition. in PLoS ONE 2013
study demonstrates that apoptosis inhibitor 5 is an endogenous and direct inhibitor of caspase-2. API5 protein directly binds to the caspase recruitment domain (CARD) of caspase-2 and impedes dimerization and activation of caspase-2.
Authors propose a proapoptotic role for NP in IAV pathogenesis, whereby it suppresses expression of antiapoptotic factor API5, thus potentiating the E2F1-dependent apoptotic pathway and ensuring viral replication.
Authors show that API5 increases the metastatic capacity of cervical cancer cells in vitro and in vivo via up-regulation of MMP-9.
rs17684886 (ZNRF1) and rs599019 (COLEC12) are associated with diabetic retinopathy and rs6427247 (SCYL1BP1) and rs899036 (API5) are associated with severe diabetic retinopathy in Chinese patients with type 2 diabetes
API5 overexpression promoted cell proliferation and colony formation in CaSki cancer cells, whereas API5 knockdown inhibited the both properties in HeLa cells; API5 expression is associated with pERK1/2 in a subset of cervical cancer patients and its expression predicts poor overall survival.
miR-143 and miR-145 and the predicted target proteins API5, ERK5, K-RAS, and IRS-1 display regional differences in expression in the colon
Negative regulation of API-5 expression by miR-1 was demonstrated to promote apoptosis of HepG2 cells.
API5 acts as an immune escape gene in tumors by rendering them resistant to apoptosis triggered by tumor antigen-specific T cells.
Low miR-224 and high API5 expression correlated with worse survival of glioblastoma patients.
Api5, even if not physically interacting with E2F1, contributes positively to E2F1 transcriptional activity by increasing E2F1 binding to its target promoters.
structure and function of API5
The prognostic significance of the genes casein kinase 2 alpha subunit (CSNK2A1), anti-apoptosis clone-11 (AAC-11), and tumor metastasis suppressor NME1 in completely resected non-small cell lung cancer (NSCLC) patients, was analysed.
we infer that Pim-2 could activate API-5 to inhibit the apoptosis of liver cells, and NF-kappaB is the key regulator
Apoptosis inhibitor-5/antiapoptosis clone-11 (Api5/Aac11) is a critical determinant of dE2F1-induced apoptosis in vivo and in vitro.
define a true in vivo target of miR-224 and reaffirm the important role of miRNAs in the dysregulation of cellular processes that may ultimately lead to tumorigenesis
The authors report here that AAC-11, a survival protein whose expression prevents apoptosis that occurs on deprivation of growth factors, physiologically binds to Acinus and prevents Acinus-mediated DNA fragmentation.
This gene encodes an apoptosis inhibitory protein whose expression prevents apoptosis after growth factor deprivation. This protein suppresses the transcription factor E2F1-induced apoptosis and also interacts with, and negatively regulates Acinus, a nuclear factor involved in apoptotic DNA fragmentation. Its depletion enhances the cytotoxic action of the chemotherapeutic drugs. Multiple alternatively spliced transcript variants encoding different isoforms have been identified.
apoptosis inhibitor 5
, Apoptosis inhibitor 5-A
, Apoptosis inhibitor 5
, apoptosis inhibitor 5-like
, antiapoptosis clone 11 protein
, cell migration-inducing gene 8 protein
, fibroblast growth factor 2-interacting factor 2
, migration-inducing protein MIG8
, apoptosis inhibitory protein 5