Recombinant Human Creb-Binding Protein (CREBBP) Protein (GST)

Name: Recombinant Human Creb-Binding Protein (CREBBP) Protein (GST)
Brand: Beta LifeScience
SKU: BLC-01525P
Availability: InStock

Greater than 85% as determined by SDS-PAGE.

Collections: All products, High-quality recombinant proteins, Other recombinant proteins

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Product Overview

Description	Recombinant Human Creb-Binding Protein (CREBBP) Protein (GST) is produced by our E.coli expression system. This is a protein fragment.
Purity	Greater than 85% as determined by SDS-PAGE.
Uniprotkb	Q92793
Target Symbol	CREBBP
Synonyms	Histone lysine acetyltransferase CREBBP;Protein-lysine acetyltransferase CREBBP
Species	Homo sapiens (Human)
Expression System	E.coli
Tag	N-GST
Target Protein Sequence	RKKIFKPEELRQALMPTLEALYRQDPESLPFRQPVDPQLLGIPDYFDIVKNPMDLSTIKRKLDTGQYQEPWQYVDDVWLMFNNAWLYNRKTSRVYKFCSKLAEVFEQEIDPVMQSLG
Expression Range	1081-1197aa
Protein Length	Partial
Mol. Weight	40.7 kDa
Research Area	Cancer
Form	Liquid or Lyophilized powder
Buffer	Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution	Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage	1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target 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-ARNTL/BMAL1 and CLOCK-ARNTL/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.
Subcellular Location	Cytoplasm. Nucleus. Note=Recruited to nuclear bodies by SS18L1/CREST. In the presence of ALX1 relocalizes from the cytoplasm to the nucleus.
Database References	HGNC: 2348 OMIM: 180849 KEGG: hsa:1387 STRING: 9606.ENSP00000262367 UniGene: PMID: 28374824 CREBBP and p300 may contribute to genome stability by fine-tuning the functions of DNA damage signaling and DNA repair factors, thereby expanding their role as tumor suppressors. (Review) PMID: 29170789 This review is focused on the different targets and functions of p300/CBP in physiological and pathological processes, including lipogenesis, lipid export, gluconeogenesis, and liver fibrosis, also provided some nutrients as the regulator of p300/CBP for nutritional therapeutic approaches to treat liver diseases. PMID: 29862292 provide evidence that both CREBBP and EP300 are bona fide tumor suppressors that control MHCII expression and promote tumor immune control; mutational inactivation of CREBBP, but not of EP300, has additional cell-intrinsic engraftment and growth-promoting effects PMID: 28831000 BRD, PHD, and ZZ domains interact with SUMO-1 and Ubc9, and function as an intramolecular E3 ligase for SUMOylation of the cell cycle regulatory domain 1; the BRD is essential for histone H3 acetylation PMID: 28630323 CREBBP Mutation is associated with Rubinstein-Taybi Syndrome and Medulloblastoma. PMID: 29551561 The recruitment of COASY inhibits CBP-mediated TPX2 acetylation, promoting TPX2 degradation for mitotic exit. PMID: 29531224 GATA3 interacts with and is acetylated by the acetyltransferase CBP. The major acetylated site of GATA3 in lung adenocarcinoma cells is lysine 119. PMID: 29453984 Our study demonstrated the association of low CREBBP expression with adverse clinical and biological features, poor prednisone response, high MRD levels and inferior outcomes in paediatric Chinese patients with ALL who were treated with the BCH- 2003 and CCLG- 2008 pro- tocols. PMID: 28452416 Knockdown of CREB suppressed the expression of matrix metallopeptidase (MMP)2/9. PMID: 28487942 mutation unlikely to be an early event in squamous cell carcinogenesis PMID: 27094574 Ectopic expression of EP300-ZNF384 and CREBBP-ZNF384 fusion altered differentiation of mouse hematopoietic stem and progenitor cells and also potentiated oncogenic transformation in vitro.our results indicate that gene fusion is a common class of genomic abnormalities in childhood ALL and that recurrent translocations involving EP300 and CREBBP may cause epigenetic deregulation with potential for therapeutic targeting. PMID: 27903646 The CREBBP acetyltransferase is a haploinsufficient tumor suppressor in B-cell lymphoma. PMID: 28069569 Understanding the effects of disrupting the acetyltransferase activity of CBP/p300 could pave the way for new therapeutic approaches to treat patients with these diseases PMID: 27380996 How cancer cells use p300/CBP in their favor varies depending on the cellular context and is evident by the growing list of loss- and gain-of-function genetic alterations in p300 and CBP in solid tumors and hematological malignancies.[review] PMID: 27881443 Mutations of CREBBP and SOCS1 are independent prognostic factors in diffuse large B cell lymphoma; CREBBP and EP300 mutations remained significant to predict worse OS, PFS, and EFS. PMID: 28302137 We conclude that patients with missense mutations in this specific CREBBP region show a phenotype that differs substantially from that in patients with Rubinstein-Taybi syndrome, and may prove to constitute one (or more) separate entities. PMID: 27311832 Pre-eclampsia occurs in 12/52 mothers of EP300 mutated individuals versus in 2/59 mothers of CREBBP mutated individuals, making pregnancy with an EP300 mutated fetus the strongest known predictor for pre-eclampsia PMID: 27648933 Earlier loss of Crebbp is advantageous for lymphoid transformation and inform the cellular origins and subsequent evolution of lymphoid malignancies. PMID: 28825697 Data show that specifically inhibiting the interaction between CBP and catenin with ICG-001 results in the differentiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs). PMID: 26657156 5-FU promotes global histone de-acetylation by enhancing the degradation of p300/CBP in colorectal neoplasms. PMID: 28465257 CREBBP mutations were associated with inferior progression-free survival (PFS), whereas mutations in previously unreported HVCN1, a voltage-gated proton channel-encoding gene and B-cell receptor signaling modulator, were associated with improved PFS. PMID: 28064239 the rate-limiting transition state for binding between the TAZ1 domain of CREB binding protein and the intrinsically disordered transactivation domain of STAT2 (TAD-STAT2) by site-directed mutagenesis and kinetic experiments (Phi-value analysis) and found that the native protein-protein binding interface is not formed at the transition state for binding. PMID: 28707474 In targeted sequencing, a disruptive mutation of TNFAIP3 was the most common alteration (54%), followed by mutations of TBL1XR1 (18%) and cAMP response element binding proteins (CREBBP) (17%). PMID: 28152507 A mosaic variant in CREBBP identified as pathogenic in a patient with overlapping clinical features of Rubinstein-Taybi and Filippi syndromes tested negative for CKAP2L. PMID: 26956253 CREBBP-BCORL1 fusion is associated with ossifying fibromyxoid tumors. PMID: 27537276 Mapping the interactions of adenoviral E1A proteins with the p160 nuclear receptor coactivator binding domain of CBP PMID: 27699893 CREBBP mutations might assist in enhancing oncogenic RAS signaling in acute lymphoblastic leukemia but do not alter response to MEK inhibitors. PMID: 27979926 Mutations identified in patients with and without classical Rubinstein-Taybi syndrome lead to skipping of exon20 of CREBBP. PMID: 27165009 Letter/Case Report: duplication mutation, c.5837dupC (p.P1947TfsX19), in CREBBP in patient with Rubinstein-Taybi syndrome with multiple pilomatricomas. PMID: 27342041 C646 treatment attenuated ETV1 protein expression and inactivated KIT-dependent pathways. Taken together, the present study suggests that CBP/p300 may serve as novel antineoplastic targets and that use of the selective HAT inhibitor C646 is a promising antitumor strategy for Gastrointestinal stromal tumors. PMID: 27633918 The CREBBP gene is believed to be the dosage-sensitive critical gene responsible for the reciprocal duplication and deletion syndrome PMID: 26873618 Results show that CREBBP was the most frequent target of epigenetic modification in juvenile myelomonocytic leukemia. PMID: 27158276 Data show that mutation of key residues in the binding site abolishes binding and that small ubiquitin-like modifier 1 (SUMO1) can simultaneously and non-cooperatively bind both the ZZ domain and a canonical SIM motif of CREB-binding protein (CBP/p300). PMID: 27129204 Cyclic AMP Response Element Binding Protein Mediates Pathological Retinal Neovascularization via Modulating DLL4-NOTCH1 Signaling PMID: 26870802 high expression of both CREB-binding protein and cleavage and polyadenylation specific factor 4 predicted a poor prognosis in the patients with lung adenocarcinomas. PMID: 26628108 RFPL3 and CBP have roles in upregulating hTERT activity and promoting lung cancer growth PMID: 26318425 Disruption of beta-catenin/CBP signaling inhibits human airway epithelial-mesenchymal transition and repair. PMID: 26315281 Intrinsic protein disorder plays a prominent role in the function and interactions of the transcriptional co-activators CBP and p300. (Review) PMID: 26851278 42 new CREBBP mutations were reported in 46 Rubinstein-Taybi syndrome patients. PMID: 25388907 Computational simulations were used to understand how phosphorylation affects the structure of the p53 terminal transactivation domain in complex with the CBP TAZ2 domain. PMID: 26742101 these data suggest that CBP/p300 are promising therapeutic targets across multiple subtypes in acute myeloid leukemia. PMID: 25893291 Conclude that the CBP/beta-catenin complex is a core component of the MDR1 transcriptional "enhancesome" in neoplasms. PMID: 25968898 WNT/beta-catenin signaling does not affect nuclear translocation of the RelA subunit of NF-kappaB or its association with CBP (also known as CREBBP) PMID: 26021349 Kaposi's sarcoma-associated herpesvirus vIRF4 targets the beta-catenin/CBP cofactor and blocks its occupancy on the cyclin D1 promoter, suppressing the G1-S cell cycle progression and enhancing virus replication. PMID: 26491150 Case Report: novel nonsense mutation of CREBBP in a patient with Rubinstein-Taybi syndrome. PMID: 26603346 destabilization of p300/CBP by downregulation of iASPP expression levels appears to represent a molecular mechanism that contributes to chemoresistance in melanoma cells. PMID: 25675294 these findings suggest that sumoylation plays a critical role in the spatiotemporal co-activation of CLOCK-BMAL1 by CBP for immediate-early Per induction and the resetting of the circadian clock. PMID: 26164627 First study of Korean Rubinstein-Taybi syndrome patients indicating distinct geographic distribution of CREBBP mutations PMID: 25108505 CREBBP mutations are associated with recurrence in hyperdiploid acute lymphoblastic leukemia. PMID: 25917266

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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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