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RFPL3 and CBP have roles in upregulating hTERT activity and promoting lung cancer growth
Disruption of beta-catenin (show CTNNB1 ELISA Kits)/CBP signaling inhibits human airway epithelial-mesenchymal transition and repair.
Intrinsic protein disorder plays a prominent role in the function and interactions of the transcriptional co-activators CBP and p300 (show EP300 ELISA Kits). (Review)
42 new CREBBP mutations were reported in 46 Rubinstein-Taybi syndrome patients.
Computational simulations were used to understand how phosphorylation affects the structure of the p53 (show TP53 ELISA Kits) terminal transactivation domain in complex with the CBP TAZ2 domain.
these data suggest that CBP/p300 are promising therapeutic targets across multiple subtypes in acute myeloid leukemia (show BCL11A ELISA Kits).
Conclude that the CBP/beta-catenin (show CTNNB1 ELISA Kits) complex is a core component of the MDR1 transcriptional "enhancesome" in neoplasms.
WNT (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling does not affect nuclear translocation of the RelA (show NFkBP65 ELISA Kits) subunit of NF-kappaB (show NFKB1 ELISA Kits) or its association with CBP (also known as CREBBP)
Kaposi's sarcoma-associated herpesvirus vIRF4 targets the beta-catenin (show CTNNB1 ELISA Kits)/CBP cofactor and blocks its occupancy on the cyclin D1 (show CCND1 ELISA Kits) promoter, suppressing the G1-S cell cycle progression and enhancing virus replication.
Case Report: novel nonsense mutation of CREBBP in a patient with Rubinstein-Taybi syndrome.
Ajuba (show AJUBA ELISA Kits) recruits p300/CBP via its LIM (show PDLIM5 ELISA Kits) domain and facilitates p300/CBP binding to PPARg (show PPARG ELISA Kits). Moreover, Ajuba (show AJUBA ELISA Kits), PPARg (show PPARG ELISA Kits), p300/CBP can cooperatively occupy the PPARg (show PPARG ELISA Kits) target promoters and concomitantly increases histone acetylation at these loci.
Recognition of the disordered TP53 (show TP53 ELISA Kits) transactivation domain by the transcriptional adapter zinc finger domains of CREB-binding protein.
Results indicate that loss of CBP CH1 domain function contributes to Rubinstein-Taybi Syndrome (RTS (show RECQL4 ELISA Kits)), and possibly Autism spectrum disorders (ASDs), and that this domain plays an essential role in normal motor function, cognition and social behavior.
Tlx3 (show TLX3 ELISA Kits) promotes glutamatergic neuronal subtype specification through direct interactions with the chromatin modifier CBP.
This study demonstrated that cbp increase in skeletal muscle in muscle atrophy.
PAG is constitutively phosphorylated in resting T cells and rapidly dephosphorylated once the TCR is engaged.
MeCP2 (show MECP2 ELISA Kits) plays an analgesic role in both acute pain transduction and chronic pain formation through regulating CREB (show CREB1 ELISA Kits)-miR (show MLXIP ELISA Kits)-132 pathway
Abeta (show APP ELISA Kits)-induced degradation of BMAL1 (show ARNTL ELISA Kits) and CBP correlated with the reduced binding of transcription factors to the Per2 (show PER2 ELISA Kits) promoter
Erythropoietin (show EPO ELISA Kits)-mediated induction of the CREBBP pathway and production of neurotrophins is associated with improved neurologic function and increased neuronal viability following spinal cord ischemia reperfusion.
If Cbp enhances the interaction between c-Src and FAK, Cbp could promote c-Src function when lipid rafts are disrupted.
This gene encodes for a light absorbing visual pigment of the opsin gene family. The encoded protein is called red cone photopigment or long-wavelength sensitive opsin. Opsins are G-protein coupled receptors with seven transmembrane domains, an N-terminal extracellular domain, and a C-terminal cytoplasmic domain. This gene and the medium-wavelength opsin gene are tandemly arrayed on the X chromosome and frequent unequal recombination and gene conversion may occur between these sequences. X chromosomes may have fusions of the medium- and long-wavelength opsin genes or may have more than one copy of these genes. Defects in this gene are the cause of partial, protanopic colorblindness.
CREB binding protein (Rubinstein-Taybi syndrome)
, CREB-binding protein
, cone dystrophy 5 (X-linked)
, long-wave-sensitive opsin 1
, red cone photoreceptor pigment
, red-sensitive opsin
, Csk-binding protein
, phosphoprotein associated with glycosphingolipid-enriched microdomains 1
, phosphoprotein transmembrane adaptor 1
, phosphoprotein-associated with GEMs
, transmembrane phosphoprotein Cbp