JUND pSer255 Rabbit Polyclonal Antibody

Specifications

Product Data
Applications	IHC, WB
Recommend Dilution	Suitable for use in Western blot (1:500~1:1000) and Immunohistochemistry on paraffin sections (1:50~1:100).
Reactivity	Human, Mouse
Host	Rabbit
Clonality	Polyclonal
Immunogen	The antiserum was produced against synthesized phosphopeptide derived from human JunD around the phosphorylation site of serine 255 (G-E-SP-P-P).
Specificity	The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific phosphopeptide. The antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site. JunD (phospho-Ser255) antibody detects endogenous levels of JunD only when phosphorylated at serine 255.
Formulation	Phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150 mM NaCl, 0.02% Sodium Azide and 50% glycerol State: Aff - Purified State: Liquid purified Ig fraction
Concentration	lot specific
Purification	Immunoaffinity chromatography
Conjugation	Unconjugated
Storage Condition	Store the antibody (in aliquots) at -20°C. Avoid repeated freezing and thawing.
Gene Name	JunD proto-oncogene, AP-1 transcription factor subunit
Database Link	Entrez Gene 3727 Human UniProt ID P17535
Background	JunD is the most broadly expressed member of the Jun family and the AP1 transcription factor complex. It has been found that primary fibroblasts lacking murine JunD displayed p53-dependent growth arrest, upregulated p19(ARF) expression, and premature senescence. In contrast, immortalized cell lines lacking JunD showed increased proliferation and higher cyclin D1 levels. These properties were reminiscent of the effects of oncogenic RAS expression on primary and established cell cultures. Furthermore, JunD -/- fibroblasts exhibited increased p53-dependent apoptosis upon ultraviolet irradiation and were sensitive to the cytotoxic effects of tumor necrosis factor-alpha. The antiapoptotic role of JunD was confirmed using an in vivo model of TNF-mediated hepatitis. The authors proposed that JunD protects cells from senescence, or apoptotic responses to stress stimuli, by acting as a modulator of the signaling pathways that link RAS to p53.
Synonyms	JUND
Reference Data

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