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The CREBBP acetyltransferase is a haploinsufficient tumor suppressor in B-cell lymphoma.
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
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 (zeige EP300 Antikörper) and CBP in solid tumors and hematological malignancies.[review]
Mutations of CREBBP and SOCS1 (zeige SOCS1 Antikörper) are independent prognostic factors in diffuse large B cell lymphoma; CREBBP and EP300 (zeige EP300 Antikörper) mutations remained significant to predict worse OS, PFS, and EFS (zeige EFS Antikörper).
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.
Pre-eclampsia occurs in 12/52 mothers of EP300 (zeige EP300 Antikörper) mutated individuals versus in 2/59 mothers of CREBBP mutated individuals, making pregnancy with an EP300 (zeige EP300 Antikörper) mutated fetus the strongest known predictor for pre-eclampsia
Earlier loss of Crebbp is advantageous for lymphoid transformation and inform the cellular origins and subsequent evolution of lymphoid malignancies.
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).
5-FU promotes global histone de-acetylation by enhancing the degradation of p300/CBP in colorectal neoplasms.
CREBBP mutations were associated with inferior progression-free survival (PFS), whereas mutations in previously unreported HVCN1 (zeige HVCN1 Antikörper), a voltage-gated proton channel-encoding gene and B-cell receptor signaling modulator, were associated with improved PFS.
Enhancer-priming by MLL3/MLL4 (zeige MLL4 Antikörper) followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation
the aPKC-CBP pathway is a homeostatic compensatory mechanism that modulates hippocampal neurogenesis and memory in an age-dependent manner in response to reduced CREB (zeige CREB1 Antikörper) activity.
High CBP-P300 expression is associated with lymphoma.
This study provides evidence from transgenic mouse models that Crebbp deletion results in deficits in B-cell development and can cooperate with Bcl2 (zeige BCL2 Antikörper) overexpression to promote B-cell lymphoma.
Data (including data from studies of hydrogen-deuterium exchange coupled to mass spectrometry in presence of denaturants) suggest that, for peptide fragments of human ACTR (zeige NCOA3 Antikörper) and mouse Crebbp representing disordered interaction domains, exchange rates are changed dramatically by high concentrations of denaturants guanidinium chloride or urea. (ACTR (zeige NCOA3 Antikörper) = activator of thyroid and retinoid receptor; Crebbp = CREB binding protein)
Crebbp+/- common myeloid progenitors and granulocyte/macrophage progenitors could trigger skewed myelopoiesis, myelodysplasia and late-onset acute myeloid leukemia (zeige BCL11A Antikörper).
Brd3 (zeige BRD3 Antikörper) knockout significantly decreased the recruitment of acetylase CBP to IL6 (zeige IL6 Antikörper) gene promoter, and the acetylation level of histone3 within IL6 (zeige IL6 Antikörper) gene promoter was repressed.
Inhibition of hypothalamic Cbp results in profound obesity and impaired glucose homeostasis, increased food intake, and decreased body temperature. In addition, these changes are accompanied by molecular evidence in the hypothalamus for impaired leptin (zeige LEP Antikörper) and insulin (zeige INS Antikörper) signaling, a shift from glucose to lipid metabolism, and decreased Pomc (zeige POMC Antikörper) mRNA, with no effect on locomotion.
Study demonstrates that CBP binds directly to RNAs in vivo and in vitro. RNAs bound to CBP in vivo include a large number of eRNAs. Using steady-state histone acetyltransferase (HAT (zeige HAT Antikörper)) assays, study shows that an RNA binding region in the HAT (zeige HAT Antikörper) domain of CBP-a regulatory motif unique to CBP/p300-allows RNA to stimulate CBP's HAT (zeige HAT Antikörper) activity.
This gene is ubiquitously expressed and is involved in the transcriptional coactivation of many different transcription factors. First isolated as a nuclear protein that binds to cAMP-response element binding protein (CREB), this gene is now known to play critical roles in embryonic development, growth control, and homeostasis by coupling chromatin remodeling to transcription factor recognition. The protein encoded by this gene has intrinsic histone acetyltransferase activity and also acts as a scaffold to stabilize additional protein interactions with the transcription complex. This protein acetylates both histone and non-histone proteins. This protein shares regions of very high sequence similarity with protein p300 in its bromodomain, cysteine-histidine-rich regions, and histone acetyltransferase domain. Mutations in this gene cause Rubinstein-Taybi syndrome (RTS). Chromosomal translocations involving this gene have been associated with acute myeloid leukemia. Alternative splicing results in multiple transcript variants encoding different isoforms.
, CREB binding protein (Rubinstein-Taybi syndrome)