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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Apoptosis inhibitor 5

FIF, API5, apoptosis inhibitor 5, AAC-11
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. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: CAN, miR, HAD, POLYMERASE, ACID
Papers on FIF
Identification of novel candidate biomarkers of epithelial ovarian cancer by profiling the secretomes of three-dimensional genetic models of ovarian carcinogenesis.
Gayther et al., London, United Kingdom. In Int J Cancer, Nov 2015
We evaluated expression of the top candidate biomarkers in ∼210 primary EOCs: CHI3L1 and FKBP4 are both expressed by >96% of primary EOCs, and FASN and API5 are expressed by 86 and 75% of cases.
Inflammatory and Immune Activation in Intestinal Myofibroblasts Is Developmentally Regulated.
Okogbule-Wonodi et al., Baltimore, United States. In J Interferon Cytokine Res, Aug 2015
The aim of this study was to further characterize differences in inflammatory signaling in human primary intestinal fibroblasts from fetal (FIF) and infant (IIF) tissue and examine their potential to activate the adaptive immune response in vitro.
iTRAQ-based quantitative subcellular proteomic analysis of Avibirnavirus-infected cells.
Zhou et al., Hangzhou, China. In Electrophoresis, Jul 2015
Confocal microscopy showed colocalization of the viral protein VP3 with host proteins heterogeneous nuclear ribonucleoprotein H1, nuclear factor 45, apoptosis inhibitor 5, nuclear protein localization protein 4 and DEAD-box RNA helicase 42 during the virus infection.
Common variants in or near ZNRF1, COLEC12, SCYL1BP1 and API5 are associated with diabetic retinopathy in Chinese patients with type 2 diabetes.
Jia et al., Shanghai, China. In Diabetologia, Jun 2015
Sub-analysis in patients with diabetic retinopathy revealed that rs6427247 near SCYL1BP1 (also known as GORAB) and rs899036 near API5 were associated with severe diabetic retinopathy (OR 1.368, p = 0.0333 and OR 0.340, p = 0.0005, respectively).
Apoptosis Inhibitor 5 Increases Metastasis via Erk-mediated MMP expression.
Kim et al., Seoul, South Korea. In Bmb Rep, Jun 2015
Apoptosis inhibitor 5 (API5) has recently been identified as a tumor metastasis-regulating gene in cervical cancer cells.
Tumor suppressors miR-143 and miR-145 and predicted target proteins API5, ERK5, K-RAS, and IRS-1 are differentially expressed in proximal and distal colon.
Bissonnette et al., Chicago, United States. In Am J Physiol Gastrointest Liver Physiol, Mar 2015
In agreement with increased expression of miR-143 and miR-145 in proximal colon, predicted targets of these miRNAs, apoptosis inhibitor 5 (API5), ERK5, K-RAS, and insulin receptor substrate 1 (IRS-1), which are cell cycle and survival regulators, were expressed at a lower level in proximal than distal colon.
MicroRNA-1 promotes apoptosis of hepatocarcinoma cells by targeting apoptosis inhibitor-5 (API-5).
Zhang et al., Chengdu, China. In Febs Lett, Feb 2015
Apoptosis inhibitor 5 (API-5) was found to be a potential regulator of miR-1 induced apoptosis, using a bioinformatics approach.
Nucleoprotein of influenza A virus negatively impacts antiapoptotic protein API5 to enhance E2F1-dependent apoptosis and virus replication.
Lal et al., New Delhi, India. In Cell Death Dis, 2014
Here we show that the nucleoprotein (NP) of IAV directly interacts with and suppresses the expression of API5, a host antiapoptotic protein that antagonizes E2F1-dependent apoptosis.
Assessing apoptosis gene expression profiling with a PCR array in the hippocampus of Ts65Dn mice.
Kong et al., Changzhou, China. In Biomed Res Int, 2014
Meanwhile, three genes (API5, AIFM1, and NFκB1) showed changes of expression in the hippocampus of Ts65Dn mice compared with normal mice.
Loss of EGFR signaling regulated miR-203 promotes prostate cancer bone metastasis and tyrosine kinase inhibitors resistance.
Kelly et al., Taipei, Taiwan. In Oncotarget, 2014
Our results demonstrate that the induction of bone metastasis and TKI resistance require miR-203 down regulation, activation of the EGFR pathway via altered expression of EGFR ligands (EREG and TGFA) and anti-apoptotic proteins (API5, BIRC2, and TRIAP1).
Prefrontal cortical and striatal transcriptional responses to the reinforcing effect of repeated methylphenidate treatment in the spontaneously hypertensive rat, animal model of attention-deficit/hyperactivity disorder (ADHD).
Cheong et al., Seoul, South Korea. In Behav Brain Funct, 2013
Pcdh10, Ctbbd1, Itgb6), positive regulation of apoptosis (Perp, Taf1, Api5), (Notch3, Nsbp1, Sik1), mitochondrion organization (Prps18c, Letm1, Uqcrc2), and ubiquitin-mediated proteolysis (Nedd4, Usp27x, Ube2d2).
Silencing BMI1 eliminates tumor formation of pediatric glioma CD133+ cells not by affecting known targets but by down-regulating a novel set of core genes.
Li et al., In Acta Neuropathol Commun, 2013
Importantly, we found that silencing BMI1 in CD133+ cells derived from 3 PDOX models did not affect most of the known genes previously associated with the activated BMI1, but modulated a novel set of core genes, including RPS6KA2, ALDH3A2, FMFB, DTL, API5, EIF4G2, KIF5c, LOC650152, C20ORF121, LOC203547, LOC653308, and LOC642489, to mediate the elimination of tumor formation.
Apoptosis inhibitor-5 overexpression is associated with tumor progression and poor prognosis in patients with cervical cancer.
Kim et al., Seoul, South Korea. In Bmc Cancer, 2013
BACKGROUND: The apoptosis inhibitor-5 (API5), anti-apoptosis protein, is considered a key molecule in the tumor progression and malignant phenotype of tumor cells.
Helical repeat structure of apoptosis inhibitor 5 reveals protein-protein interaction modules.
Lee et al., South Korea. In J Biol Chem, 2012
structure and function of API5
Gene expression levels of CSNK1A1 and AAC-11, but not NME1, in tumor tissues as prognostic factors in NSCLC patients.
Zhou et al., Tianjin, China. In Med Sci Monit, 2010
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.
Pim-2 activates API-5 to inhibit the apoptosis of hepatocellular carcinoma cells through NF-kappaB pathway.
Gong et al., Chongqing, China. In Pathol Oncol Res, 2010
we infer that Pim-2 could activate API-5 to inhibit the apoptosis of liver cells, and NF-kappaB is the key regulator
Targeting AAC-11 in cancer therapy.
Poyet et al., Paris, France. In Expert Opin Ther Targets, 2010
IMPORTANCE OF THE FIELD: Since its discovery in 1997, the antiapoptotic factor AAC-11 has rapidly gained attention due to its potential use in cancer therapy.
The antiapoptotic protein AAC-11 interacts with and regulates Acinus-mediated DNA fragmentation.
Poyet et al., Paris, France. In Embo J, 2009
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.
Profiling microRNA expression in hepatocellular carcinoma reveals microRNA-224 up-regulation and apoptosis inhibitor-5 as a microRNA-224-specific target.
Lee et al., Singapore, Singapore. In J Biol Chem, 2008
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
[Sociohygienic monitoring in the Russian Federation: problems and tasks].
Onishchenko, In Gig Sanit, 2006
Much work has been recently done to establish and manage a federal information fund (FIF) that is a database on the human health status and environment, based on long-term observations and an aggregate of normative legal acts and reference materials on the analysis of prediction and determination of cause-and-effect relations between the human health status and the influence of environmental factors.
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