SAB4503405
Anti-HAT antibody produced in rabbit
affinity isolated antibody
Synonym(e):
KAT1, histone acetyltransferase 1, histone acetyltransferase type B catalytic
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About This Item
UNSPSC-Code:
12352203
NACRES:
NA.41
Empfohlene Produkte
Biologische Quelle
rabbit
Konjugat
unconjugated
Antikörperform
affinity isolated antibody
Antikörper-Produkttyp
primary antibodies
Klon
polyclonal
Form
buffered aqueous solution
Mol-Gew.
antigen 49 kDa
Speziesreaktivität
mouse, rat, human
Konzentration
~1 mg/mL
Methode(n)
ELISA: 1:5000
western blot: 1:500-1:1000
NCBI-Hinterlegungsnummer
UniProt-Hinterlegungsnummer
Versandbedingung
wet ice
Lagertemp.
−20°C
Posttranslationale Modifikation Target
unmodified
Angaben zum Gen
human ... HAT1(8520)
Verwandte Kategorien
Allgemeine Beschreibung
Histone acetyltransferase 1 (HAT1) is a type B histone acetyltransferase localized in the cytosol and the nucleus. The HAT1 gene is mapped on the human chromosome at 2q31.1.
Immunogen
The antiserum was produced against synthesized peptide derived from human HAT.
Immunogen Range: 331-380
Immunogen Range: 331-380
Anwendung
Anti-HAT antibody produced in rabbit has been used in western blotting (1:500) and immunofluorescence (1:250).
Biochem./physiol. Wirkung
Histone acetyltransferase 1 (HAT1) is involved in the acetylation of lysine 5- and 12- residues at the N-terminal of the newly synthesized histone H4. This enzyme is also involved in the regulation of DNA repair in the nucleus.
Leistungsmerkmale und Vorteile
Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.
Physikalische Form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Haftungsausschluss
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Lagerklassenschlüssel
10 - Combustible liquids
WGK
nwg
Flammpunkt (°F)
Not applicable
Flammpunkt (°C)
Not applicable
Analysenzertifikate (COA)
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Xiaohan Yang et al.
The Journal of biological chemistry, 288(25), 18271-18282 (2013-05-09)
Faithful repair of DNA double-strand breaks is vital to the maintenance of genome integrity and proper cell functions. Histone modifications, such as reversible acetylation, phosphorylation, methylation, and ubiquitination, which collectively contribute to the establishment of distinct chromatin states, play important
Hirak Kumar Barman et al.
Biochemical and biophysical research communications, 373(4), 624-630 (2008-07-08)
Amounts of soluble histones in cells are tightly regulated to ensure supplying them for the newly synthesized DNA and preventing the toxic effect of excess histones. Prior to incorporation into chromatin, newly synthesized histones H3 and H4 are highly acetylated
Svetlana Demyanenko et al.
International journal of molecular sciences, 20(12) (2019-06-16)
Ischemic penumbra that surrounds a stroke-induced infarction core is potentially salvageable; however, mechanisms of its formation are not well known. Covalent modifications of histones control chromatin conformation, gene expression and protein synthesis. To study epigenetic processes in ischemic penumbra, we
Yueqin Wang et al.
Chemosphere, 241, 125073-125073 (2019-11-07)
Microcystin-leucine arginine (MC-LR) is a variant of microcystins (MCs), which poses a serious threat to the reproductive system. Histone acetylation modification can regulate the expressions of apoptosis-related genes. However the mechanisms of histone acetylation involving MC-LR-induced apoptosis were not understood.
S V Demyanenko et al.
Molecular neurobiology, 57(7), 3219-3227 (2020-06-09)
Stroke is one of the leading reasons of human death. Ischemic penumbra that surrounds the stroke-induced infarction core is potentially salvageable, but molecular mechanisms of its formation are poorly known. Histone acetylation induces chromatin decondensation and stimulates gene expression. We
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