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PML-RARA regulated adaptor molecule 1

The protein encoded by this gene is similar to FYN binding protein (FYB/SLAP-130), an adaptor protein involved in T cell receptor mediated signaling. This gene is expressed and regulated during normal myelopoiesis. The expression of this gene is induced by retinoic acid and is inhibited by the expression of PML-RARalpha, a fusion protein of promyelocytic leukemia (PML) and the retinoic acid receptor-alpha (RARalpha). [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PML, RAR, ACID, CAN, POLYMERASE
Papers on PML-RAR
Activity-related parenting practices: development of the Parenting Related to Activity Measure (PRAM) and links with mothers' eating psychopathology and compulsive exercise beliefs.
Meyer et al., Loughborough, United Kingdom. In Eur Eat Disord Rev, 2015
This is a two-study paper that developed a measure to assess parenting practices related to children's physical activity and explored maternal predictors of such parenting practices.
Lattice Distortion in In3SbTe2 Phase Change Material with Substitutional Bi.
Kim et al., South Korea. In Sci Rep, 2014
Consequently, phase change random access memory (PRAM) fabricated with Bi-doped IST (Bi-IST) can operate with lower power consumption than pure IST PRAM.
Extrinsic apoptosis is impeded by direct binding of the APL fusion protein NPM-RAR to TRADD.
Redner et al., Pittsburgh, United States. In Mol Cancer Res, 2014
The resultant NPM-RAR fusion protein blocks myeloid differentiation and leads to a leukemic phenotype similar to that caused by the t(15;17)(q22;q21) PML-RAR fusion.
Autologous is superior to allogeneic hematopoietic cell transplantation for acute promyelocytic leukemia in second complete remission.
Tallman et al., Winnipeg, Canada. In Biol Blood Marrow Transplant, 2014
Positive pre-HCT PML-RAR∝ status in 17 of 114 allogeneic and 6 of 41 receiving autologous transplantation did not influence relapse, treatment failure, or survival in either group.
Identifying Yersinia YopH-targeted signal transduction pathways that impair neutrophil responses during in vivo murine infection.
Mecsas et al., Boston, United States. In Cell Host Microbe, 2013
YopH inactivated PRAM-1/SKAP-HOM and the SLP-76/Vav/PLCγ2 signal transduction axes, leading to an inhibition of calcium response in isolated neutrophils.
A new era for an ancient drug: arsenic trioxide and Hedgehog signaling.
Uren et al., Washington, D.C., United States. In Vitam Horm, 2011
Currently, it is an FDA approved drug to treat acute promyelocytic leukemia where it leads to degradation of the PML-RAR fusion protein.
PML-RARα enhances constitutive autophagic activity through inhibiting the Akt/mTOR pathway.
Chen et al., Shanghai, China. In Autophagy, 2011
autophagy contributes to the anti-apoptotic function of the PML-RARalpha protein through inhibiting the Akt/mTOR pathway
Genome-wide functions of PML-RARα in acute promyelocytic leukaemia.
Martens et al., Nijmegen, Netherlands. In Br J Cancer, 2011
PML-RAR (retinoic acid receptor)α is the hallmark protein of acute promyelocytic leukaemia, a highly malignant subtype of acute myeloid leukaemia that accounts for approximately 10% of all AML cases.
Unusual acute promyelocytic leukemia following de novo renal transplant: case report and literature review.
Chen et al., Taiwan. In Clin Nephrol, 2011
Acute promyelocytic leukemia (APL) with transcripting three isoforms of mRNA from PML-RAR alpha fusion genes following renal transplantation has never been reported in the literature.
Interplay of protein misfolding pathway and unfolded-protein response in acute promyelocytic leukemia.
Khan, Singapore, Singapore. In Expert Rev Proteomics, 2010
PML-RAR promotes misfolding of N-CoR by inducing aberrant post-translational modification, which destabilizes its core and promotes instability.
Hidden abnormalities and novel classification of t(15;17) acute promyelocytic leukemia (APL) based on genomic alterations.
Koeffler et al., Los Angeles, United States. In Blood, 2009
hidden abnormalities and novel disease-related genomic changes occur in t(15;17)translocation in acute promyelocytic leukemia formation of PML-RARA gene
Quantitative detection of PML-RARalpha fusion transcript by real-time PCR with a single primer pair.
Kumagai et al., Himeji, Japan. In J Clin Lab Anal, 2008
We conclude that our sp-RQ-PCR is specific enough to identify various forms of PML-RARalpha and yields no false-positive results.
Lipid-binding hSH3 domains in immune cell adapter proteins.
Freund et al., Berlin, Germany. In J Mol Biol, 2006
Interaction of PRAM-1 and hSH3 domains of adhesion and degranulation promoting adapter protein (ADAP) with phosphatidylcholine-containing liposomes is observed upon incorporation of phosphatidylserine or phosphoinositides into the membrane bilayer.
Diagnosis and monitoring of PML-RARalpha-positive acute promyelocytic leukemia by quantitative RT-PCR.
Applegate et al., Australia. In Methods Mol Med, 2005
PML-RARalpha fusion transcripts have been shown to be useful markers for establishing the diagnosis and for monitoring the response to treatment of acute promyelocytic leukemia.
Inhibitors of histone deacetylases induce tumor-selective apoptosis through activation of the death receptor pathway.
Pelicci et al., Milano, Italy. In Nat Med, 2005
We investigated the effects of HDACIs on leukemias expressing the PML-RAR or AML1-ETO oncoproteins, known to initiate leukemogenesis through deregulation of HDACs.
Leukemia: stem cells, maturation arrest, and differentiation therapy.
Sell, Albany, United States. In Stem Cell Rev, 2004
In acute promyelocytic leukemia, fusion of the retinoic acid receptor-alpha with the gene coding for promyelocytic protein, the PML-RAR alpha (t15:17) translocation, produces a fusion product that blocks the activity of the promyelocytic protein, which is required for formation of the granules of promyelocytes and prevents further differentiation.
Methyltransferase recruitment and DNA hypermethylation of target promoters by an oncogenic transcription factor.
Pelicci et al., Milano, Italy. In Science, 2002
We report here that the leukemia-promoting PML-RAR fusion protein induces gene hypermethylation and silencing by recruiting DNA methyltransferases to target promoters and that hypermethylation contributes to its leukemogenic potential.
Complete remission after treatment of acute promyelocytic leukemia with arsenic trioxide.
Warrell et al., New York City, United States. In N Engl J Med, 1998
Bone marrow mononuclear cells were serially monitored by flow cytometry for immunophenotype, fluorescence in situ hybridization, reverse-transcription-polymerase-chain-reaction (RT-PCR) assay for PML-RAR-alpha fusion transcripts, and Western blot analysis for expression of the apoptosis-associated proteins caspases 1, 2, and 3. RESULTS: Of the 12 patients studied, 11 achieved complete remission after treatment that lasted from 12 to 39 days (range of cumulative doses, 160 to 495 mg).
PML is essential for multiple apoptotic pathways.
Pandolfi et al., New York City, United States. In Nat Genet, 1998
The PML-RAR alpha fusion protein of APL renders haemopoietic progenitor cells resistant to Fas-, TNF- and IFN-induced apoptosis with a lack of caspase 3 activation, thus acting as a Pml dominant-negative product.
Secondary cytogenetic changes in acute promyelocytic leukemia--prognostic importance in patients treated with chemotherapy alone and association with the intron 3 breakpoint of the PML gene: a Cancer and Leukemia Group B study.
Bloomfield et al., Buffalo, United States. In J Clin Oncol, 1997
PURPOSE: To examine, in newly diagnosed patients with acute promyelocytic leukemia (APL), the prognostic significance of secondary cytogenetic changes and the relationship between such changes and the two major promyelocytic leukemia-retinoic acid receptor alpha (PML-RAR alpha) mRNA types.
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