Monkey CREB binding Protein(CREBBP) ELISA Kit (RMEK-0153198)
Cat. No.: RMEK-0153198
Category: ELISA Kits
INQUIRY
1 x 96 tests
This ELISA kit is a 1. 5 hour solid-phase ELISA designed for the quantitative determination of the targets. This ELISA kit for research use only, not for therapeutic or diagnostic applications!
Product Features
| Species Reactivity | Monkey |
|---|---|
| Assay Time | 1.5 h |
Target Information
| Target Symbol | CREBBP |
|---|---|
| UniProt ID | Q92793 |
| Biomarker of SCs/CSCs | Pancreatic Cancer |
| Function | Acetylates histones, giving a specific tag for transcriptional activation. Also acetylates non-histone proteins, like DDX21, FBL, IRF2, MAFG, NCOA3, POLR1E/PAF53 and FOXO1. Binds specifically to phosphorylated CREB and enhances its transcriptional activity toward cAMP-responsive genes. Acts as a coactivator of ALX1. Acts as a circadian transcriptional coactivator which enhances the activity of the circadian transcriptional activators: NPAS2-BMAL1 and CLOCK-BMAL1 heterodimers. Acetylates PCNA; acetylation promotes removal of chromatin-bound PCNA and its degradation during nucleotide excision repair (NER). Acetylates POLR1E/PAF53, leading to decreased association of RNA polymerase I with the rDNA promoter region and coding region. Acetylates DDX21, thereby inhibiting DDX21 helicase activity. Acetylates FBL, preventing methylation of 'Gln-105' of histone H2A (H2AQ104me). Functions as a transcriptional coactivator for SMAD4 in the TGF-beta signaling pathway. |
| Cellular Localization | Cytoplasm. Nucleus. Recruited to nuclear bodies by SS18L1/CREST. In the presence of ALX1 relocalizes from the cytoplasm to the nucleus. |
| Domain | The KIX domain mediates binding to HIV-1 Tat. |
| Post-transcriptional Modifications | Methylation of the KIX domain by CARM1 blocks association with CREB. This results in the blockade of CREB signaling, and in activation of apoptotic response (By similarity). Phosphorylated by CHUK/IKKA at Ser-1382 and Ser-1386; these phosphorylations promote cell growth by switching the binding preference of CREBBP from TP53 to NF-kappa-B. Sumoylation negatively regulates transcriptional activity via the recruitment of DAAX. Autoacetylation is required for binding to protein substrates, such as acetylated histones and acetylated TP53/p53. Autoacetylation is induced by glucose and fatty acids. |
| Involvement in Disease | Chromosomal aberrations involving CREBBP may be a cause of acute myeloid leukemias. Translocation t(8; 16)(p11; p13) with KAT6A; translocation t(11; 16)(q23; p13. 3) with KMT2A/mLL1; translocation t(10; 16)(q22; p13) with KAT6B. KAT6A-CREBBP may induce leukemia by inhibiting RUNX1-mediated transcription. Rubinstein-Taybi syndrome 1 (RSTS1): A disorder characterized by craniofacial abnormalities, postnatal growth deficiency, broad thumbs, broad big toes, intellectual disability and a propensity for development of malignancies. The disease is caused by variants affecting the gene represented in this entry. Menke-Hennekam syndrome 1 (MKHK1): A form of Menke-Hennekam syndrome, a congenital autosomal dominant disease characterized by developmental delay, growth retardation, and craniofacial dysmorphism. Patients have intellectual disability of variable severity, speech delay, autistic behavior, short stature and microcephaly. Main facial characteristics include short palpebral fissures, telecanthi, depressed nasal ridge, short nose, anteverted nares, short columella and long philtrum. The disease is caused by variants affecting the gene represented in this entry. |
Storage & Shipping
| Storage | Store at 2-8°C |
|---|---|
| Shipping | Gel Packs |
| Stability | The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. |
For research use only. Not for clinical use.
