Anti-Acetyl-Histone H2B (Lys12) Rabbit pAb
PTM-108
ApplicationsWestern Blot, ChIP Chromatin ImmunoPrecipitation
Product group Antibodies
ReactivityHuman, Mouse, Rat
Overview
- SupplierPTM BIO
- Product NameAnti-Acetyl-Histone H2B (Lys12) Rabbit pAb
- Delivery Days Customer5
- Antibody SpecificityAnti-Acetyl-Histone H2B (Lys12) Rabbit pAb detects histone H2B only when it is acetylated at Lys12. This antibody has been shown to selectively recognize acetylated H2B peptide at Lys12, but not the structurally similar crotonylated peptides at Lys11 or Lys12.
- ApplicationsWestern Blot, ChIP Chromatin ImmunoPrecipitation
- Applications SupplierWB, ChIP
- Category SupplierAntibody
- CertificationResearch Use Only
- ClonalityPolyclonal
- ConjugateUnconjugated
- HostRabbit
- IsotypeIgG
- Protein IDP62807
- Protein NameHistone H2B type 1-C/E/F/G/I
- Scientific DescriptionHistone post-translational modifications (PTMs), known as the “histone code”, are key mechanisms of epigenetics that modulate chromatin structures. The PTMs on histone including acetylation, methylation, Phosphorylatedrylation, and novel acylations directly affect the accessibility of chromatin to transcription factors and other epigenetic regulators, altering genome stability and gene transcription. Histone acetylation, tightly controlled by the opposing action of histone acetyltransferases (HATs) and histone deacetylases (HDACs), occurs primarily at lysine residues on the N-terminal tails of histones H2A (Lys5, 9, and 15), H2B (Lys5,12, 15, 16, and 20), H3 (Lys4, 9, 14, 18, 23, 27, and 36), and H4 (Lys5, 8, 12, 16, and 20), and plays vital roles in the regulation of gene expression, DNA damage repair, chromatin dynamics, etc.
- Shelf life instructionStable for 12 months from date of receipt/reconstitution.
- ReactivityHuman, Mouse, Rat
- Reactivity SupplierHuman, Mouse, Rat
- Reactivity Supplier NoteProtein A and immunogen affinity purified
- Storage InstructionStore at -20°C. Avoid freeze/thaw cycles.
- UNSPSC12352203
References
- Pan Botao, et al. 'Activation of AMPK inhibits cervical cancer growth by hyperacetylation of H3K9 through PCAF' Cell Communication and Signaling (2024)Read more