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Retinoblastoma binding protein 5

SwDI, Rbbp5, retinoblastoma binding protein-5
This gene encodes a ubiquitously expressed nuclear protein which belongs to a highly conserved subfamily of WD-repeat proteins. The encoded protein binds directly to retinoblastoma protein, which regulates cell proliferation. It interacts preferentially with the underphosphorylated retinoblastoma protein via the E1A-binding pocket B. Three alternatively spliced transcript variants that encode different protein isoforms have been described for this gene. [provided by RefSeq, Jul 2010] (from NCBI)
Top mentioned proteins: APP, Histone, ASH2, CAN, AGE
Papers using SwDI antibodies
A single lentiviral vector platform for microRNA-based conditional RNA interference and coordinated transgene expression.
Lee Jeannie T., In PLoS Genetics, 2005
... Antibodies against RNF20 (A300-715A) and RBBP5 (A300-109A) were obtained from Bethyl Laboratories ...
Summaries of Affymetrix GeneChip probe level data
Snyder Michael, In PLoS Genetics, 2002
... Affinity-purified rabbit polyclonal anti-menin (BL342), anti-Rbbp5 (BL766), and anti-MLL1 (BL1289) antibodies were obtained from Bethyl Laboratories (Montgomery, Texas, United ...
Papers on SwDI
Expression and clinical role of RBQ3 in gliomas.
Ren et al., Nantong, China. In J Neurol Sci, Jan 2016
RBQ3, also known as RBBP5 (RB-binding protein 5), was an RB-binding protein.
Deficits in hippocampal-dependent transfer generalization learning accompany synaptic dysfunction in a mouse model of amyloidosis.
Bizon et al., East Orange, United States. In Hippocampus, Oct 2015
Finally, Experiment 3 confirmed that the same transfer learning impairments observed in APPswePS1 mice were also evident in the Tg-SwDI mouse, a second model of amyloidosis.
PAQR3 modulates H3K4 trimethylation by spatial modulation of the regulatory subunits of COMPASS-like complexes in mammalian cells.
Chen et al., Shanghai, China. In Biochem J, Jun 2015
H3K4 methylation in mammalian cells is carried out by COMPASS (complex of proteins associated with Set1)-like complexes that are composed of catalytic subunits such as MLL1 (mixed-lineage leukaemia 1) and multiple regulatory subunits in which WDR5 (WD40 repeat-containing protein 5), RBBP5 (retinoblastoma-binding protein 5), ASH2 (absent, small or homoeotic discs 2) and DPY30 [constituting the WRAD sub-complex (WDR5-ASH2-RBBP5-DPY30 complex)] are the major ones shared from yeast to metazoans.
Biochemical reconstitution and phylogenetic comparison of human SET1 family core complexes involved in histone methylation.
Cosgrove et al., Syracuse, United States. In J Biol Chem, Apr 2015
MLL1 assembles with WDR5, RBBP5, ASH2L, DPY-30 (WRAD) to form the MLL1 core complex, which is required for H3K4 dimethylation and transcriptional activation.
Phosphodiesterase III inhibitor promotes drainage of cerebrovascular β-amyloid.
Ihara et al., Kyoto, Japan. In Ann Clin Transl Neurol, 2014
METHODS: We explored the expression of PDE III in postmortem human brain tissue followed by a series of experiments examining the effects of cilostazol on Aβ metabolism in transgenic mice (Tg-SwDI mice) as a model of cerebrovascular β-amyloidosis, as well as cultured neurons.
Epigenetically modulated LRRC33 acts as a negative physiological regulator for multiple Toll-like receptors.
Yang et al., Beijing, China. In J Leukoc Biol, 2014
Furthermore, silencing H3K4me3-associated factors MLL and RBBP5 not only decreased the enrichment of H3K4me3 but also down-regulated expression of LRRC33, whereas the expression of LRRC33 was up-regulated after silencing H3K27me3-associated factors EZH2 and EED.
Early-onset formation of parenchymal plaque amyloid abrogates cerebral microvascular amyloid accumulation in transgenic mice.
Van Nostrand et al., Stony Brook, United States. In J Biol Chem, 2014
Tg-5xFAD mice, which produce non-mutated human Aβ and develop early-onset parenchymal amyloid plaques, were bred to Tg-SwDI mice, which produce familial CAA mutant human Aβ and develop cerebral microvascular amyloid.
Age-dependent neurovascular dysfunction and damage in a mouse model of cerebral amyloid angiopathy.
Iadecola et al., Chile. In Stroke, 2014
METHODS: We used male transgenic mice expressing the Swedish, Iowa, and Dutch mutations of the amyloid precursor protein (Tg-SwDI) to examine the effect of cerebral amyloid angiopathy on cerebrovascular structure and function.
Dihydromyricetin ameliorates behavioral deficits and reverses neuropathology of transgenic mouse models of Alzheimer's disease.
Olsen et al., Los Angeles, United States. In Neurochem Res, 2014
In this study, transgenic (TG2576) and Swedish transgenic (TG-SwDI) mice with AD-like pathology were treated with DHM (2 mg/kg) for 3 months.
WDR5, ASH2L, and RBBP5 control the efficiency of FOS transcript processing.
Sharrocks et al., Kota Kinabalu, Malaysia. In Cell Mol Biol Lett, 2014
The deposition of this mark is catalyzed by SET-domain methyltransferases, which consist of a subcomplex containing WDR5, ASH2L, and RBBP5 (the WAR subcomplex); a catalytic SET-domain protein; and additional complexspecific subunits.
Impact of age on the cerebrovascular proteomes of wild-type and Tg-SwDI mice.
Horsburgh et al., Edinburgh, United Kingdom. In Plos One, 2013
Over 650 proteins were quantified in vessel-enriched fractions from the brains of 3 and 9 month-old wild-type (WT) and Tg-SwDI mice.
FBP1 Is an Interacting Partner of Menin.
Marx et al., Bethesda, United States. In Int J Endocrinol, 2013
We describe the identification of FBP1 as an interacting partner of menin in a large-scale pull-down assay that also immunoprecipitated RBBP5, ASH2, and LEDGF, which are members of complex proteins associated with SET1 (COMPASS), a protein complex that methylates histone H3.
Integrated multi-cohort transcriptional meta-analysis of neurodegenerative diseases.
Khatri et al., In Acta Neuropathol Commun, 2013
ENCODE ChIP-seq analysis predicted common upstream transcriptional regulators not associated with normal aging (REST, RBBP5, SIN3A, SP2, YY1, ZNF143, IKZF1).
Dendritic cell-associated miRNAs are modulated via chromatin remodeling in response to different environments.
Yang et al., Tianjin, China. In Plos One, 2013
siRNAs targeting H3K4me3-associated mixed lineage leukemia (MLL) and retinoblastoma binding protein 5 (RBBP5) reduced H3K4me3 enrichment and downregulated miRNA expression; conversely, silencing H3K27me3-associated enhancer of zeste homolog 2 (EZH2) and embryonic ectoderm development (EED) genes upregulated the DC-associated miRNAs.
Carm1 regulates Pax7 transcriptional activity through MLL1/2 recruitment during asymmetric satellite stem cell divisions.
Rudnicki et al., Ottawa, Canada. In Cell Stem Cell, 2012
Methylated Pax7 directly binds the C-terminal cleavage forms of the trithorax proteins MLL1/2 resulting in the recruitment of the ASH2L:MLL1/2:WDR5:RBBP5 histone H3K4 methyltransferase complex to regulatory enhancers and the proximal promoter of Myf5.
Structure of the SPRY domain of human Ash2L and its interactions with RbBP5 and DPY30.
Lei et al., In Cell Res, 2012
structural and biochemical analyses reveal a basic surface on Ash2L as the RbBP5-binding interface, and this interface is crucial for both RbBP5 binding and MLL1 methyltransferase activity regulation
Regulation of HOXA2 gene expression by the ATP-dependent chromatin remodeling enzyme CHD8.
Bochar et al., Ann Arbor, United States. In Febs Lett, 2010
Results show that Depletion of CHD8 enhances HOXA2 expression and a loss of the WDR5/Ash2L/RbBP5 subcomplex.
An Ash2L/RbBP5 heterodimer stimulates the MLL1 methyltransferase activity through coordinated substrate interactions with the MLL1 SET domain.
Dou et al., Ann Arbor, United States. In Plos One, 2009
MLL1 SET domain make direct contacts with the substrates and contribute to the formation of a joint catalytic center.
Genome-wide analysis of menin binding provides insights into MEN1 tumorigenesis.
Collins et al., Bethesda, United States. In Plos Genet, 2006
analysis of menin's role as a tumor suppressor and binding sites of Rbbp5 and MLL1
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