Anti-KAT3B / p300 antibody, prediluted (ab41840)

Overview

  • Product nameAnti-KAT3B / p300 antibody, predilutedSee all KAT3B / p300 primary antibodies ...
  • Description
    Rabbit polyclonal to KAT3B / p300, prediluted
  • Tested applicationsIHC-Pmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Mouse, Rat
  • Immunogen

    Synthetic peptide corresponding to C-terminal region of human p300. The amino acid sequence is unavailable.

  • Positive control
    • Breast carcinoma.

Properties

Applications

Our Abpromise guarantee covers the use of ab41840 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P
  • Application notesIHC-P: Ready-to-use. 30 min at RT. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.

    Not yet tested in other applications.
    Optimal dilutions/concentrations should be determined by the end user.
  • Target

    • FunctionFunctions as histone acetyltransferase and regulates transcription via chromatin remodeling. Acetylates all four core histones in nucleosomes. Histone acetylation gives an epigenetic tag for transcriptional activation. Mediates cAMP-gene regulation by binding specifically to phosphorylated CREB protein. Also functions as acetyltransferase for nonhistone targets. Acetylates 'Lys-131' of ALX1 and acts as its coactivator in the presence of CREBBP. Acetylates SIRT2 and is proposed to indirectly increase the transcriptional activity of TP53 through acetylation and subsequent attenuation of SIRT2 deacetylase function. Acetylates HDAC1 leading to its inactivation and modulation of transcription. Acts as a TFAP2A-mediated transcriptional coactivator in presence of CITED2. Plays a role as a coactivator of NEUROD1-dependent transcription of the secretin and p21 genes and controls terminal differentiation of cells in the intestinal epithelium. Promotes cardiac myocyte enlargement. Can also mediate transcriptional repression. Binds to and may be involved in the transforming capacity of the adenovirus E1A protein. In case of HIV-1 infection, it is recruited by the viral protein Tat. Regulates Tat's transactivating activity and may help inducing chromatin remodeling of proviral genes. Acetylates FOXO1 and enhances its transcriptional activity.
    • Involvement in diseaseNote=Defects in EP300 may play a role in epithelial cancer.
      Note=Chromosomal aberrations involving EP300 may be a cause of acute myeloid leukemias. Translocation t(8;22)(p11;q13) with KAT6A.
      Rubinstein-Taybi syndrome 2 (RSTS2) [MIM:613684]: A disorder characterized by craniofacial abnormalities, postnatal growth deficiency, broad thumbs, broad big toes, mental retardation and a propensity for development of malignancies. Some individuals with RSTS2 have less severe mental impairment, more severe microcephaly, and a greater degree of changes in facial bone structure than RSTS1 patients. Note=The disease is caused by mutations affecting the gene represented in this entry.
    • Sequence similaritiesContains 1 bromo domain.
      Contains 1 KIX domain.
      Contains 2 TAZ-type zinc fingers.
      Contains 1 ZZ-type zinc finger.
    • DomainThe CRD1 domain (cell cycle regulatory domain 1) mediates transcriptional repression of a subset of p300 responsive genes; it can be de-repressed by CDKN1A/p21WAF1 at least at some promoters. It conatins sumoylation and acetylation sites and the same lysine residues may be targeted for the respective modifications. It is proposed that deacetylation by SIRT1 allows sumoylation leading to suppressed activity.
    • Post-translational
      modifications
      Acetylated on Lys at up to 17 positions by intermolecular autocatalysis. Deacetylated in the transcriptional repression domain (CRD1) by SIRT1, preferentially at Lys-1020.
      Citrullinated at Arg-2142 by PADI4, which impairs methylation by CARM1 and promotes interaction with NCOA2/GRIP1.
      Methylated at Arg-580 and Arg-604 in the KIX domain by CARM1, which blocks association with CREB, inhibits CREB signaling and activates apoptotic response. Also methylated at Arg-2142 by CARM1, which impairs interaction with NCOA2/GRIP1.
      Sumoylated; sumoylation in the transcriptional repression domain (CRD1) mediates transcriptional repression. Desumoylated by SENP3 through the removal of SUMO2 and SUMO3.
      Probable target of ubiquitination by FBXO3, leading to rapid proteasome-dependent degradation.
      Phosphorylated by HIPK2 in a RUNX1-dependent manner. This phosphorylation that activates EP300 happens when RUNX1 is associated with DNA and CBFB. Phosphorylated by ROCK2 and this enhances its activity. Phosphorylation at Ser-89 by AMPK reduces interaction with nuclear receptors, such as PPARG.
    • Cellular localizationCytoplasm. Nucleus. In the presence of ALX1 relocalizes from the cytoplasm to the nucleus. Co-localizes with ROCK2 in the nucleus.
    • Information by UniProt
    • Database links
    • Alternative names
      • CREBBP/EP300 inhibitory protein 1 antibody
      • CREBBP/EP300 inhibitory protein 1 antibody
      • Cyclic AMP responsive enhancer binding protein antibody
      • E1A associated protein p300 antibody
      • E1A binding protein p300 antibody
      • E1A-associated protein p300 antibody
      • EC 2.3.1.48 antibody
      • EP300 antibody
      • EP300: E1A binding protein p300 antibody
      • EP300: E1A binding protein p300 antibody
      • EP300_HUMAN antibody
      • Histone acetyltransferase p300 antibody
      • p300 HAT antibody
      • RB and P300 binding protein EID 1 antibody
      • Retinoblastoma protein associated protein antibody
      • RSTS2 antibody
      see all

    Anti-KAT3B / p300 antibody, prediluted images

    • Ab41840 staining human p300 in human breast carcinoma by immunohistochemistry using formalin fixed, paraffin embedded tissue.

    References for Anti-KAT3B / p300 antibody, prediluted (ab41840)

    ab41840 has not yet been referenced specifically in any publications.

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