1. Since applications vary, each investigator should titrate the reagent to obtain optimal results. 2. Please refer to us for technical protocols. 3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
纯化方法
The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography.
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
储存条件
4 °C
储存方法
Store undiluted at 4° C.
Zhu, Jiang, Zhou, Chen: "The potential tumor suppressor p73 differentially regulates cellular p53 target genes." in: Cancer research, Vol. 58, Issue 22, pp. 5061-5, (1998) (PubMed).
De Laurenzi, Costanzo, Barcaroli, Terrinoni, Falco, Annicchiarico-Petruzzelli, Levrero, Melino: "Two new p73 splice variants, gamma and delta, with different transcriptional activity." in: The Journal of experimental medicine, Vol. 188, Issue 9, pp. 1763-8, (1998) (PubMed).
Marin, Jost, Irwin, DeCaprio, Caput, Kaelin: "Viral oncoproteins discriminate between p53 and the p53 homolog p73." in: Molecular and cellular biology, Vol. 18, Issue 11, pp. 6316-24, (1998) (PubMed).
Jost, Marin, Kaelin: "p73 is a simian [correction of human] p53-related protein that can induce apoptosis." in: Nature, Vol. 389, Issue 6647, pp. 191-4, (1997) (PubMed).
Kaghad, Bonnet, Yang, Creancier, Biscan, Valent, Minty, Chalon, Lelias, Dumont, Ferrara, McKeon, Caput: "Monoallelically expressed gene related to p53 at 1p36, a region frequently deleted in neuroblastoma and other human cancers." in: Cell, Vol. 90, Issue 4, pp. 809-19, (1997) (PubMed).
抗原
Tumor Protein p73 (TP73)
(Tumor Protein P73 (TP73))
P53 is a tumor suppressor which acts as an S-phase checkpoint for DNA damage. The gene for p53 is the most commonly mutated gene identified in human cancers. Recently, a new member of the p53 family, p73, was identified. p73 is structurally homologous to p53 in several regions, including the p53 N-terminal transactivation domain and C-terminal oligomerization domains, as well as the region corresponding to the p53 DNA-binding domain. When overexpressed, p73 can promote p53-like functions, including induction of apoptosis and induction of transcription from p53-responsive promoters such as p21. Despite structural and apparent functional homology, data suggests that these proteins may have distinct functions as well. For example, viral oncoproteins such as Adenovirus E1B 55K and HPV E6, which bind to and thus inactivate p53 during the process of transformation, do not bind to p73. In addition, unlike p53, p73 expression is not induced by DNA damage, e.g. UV irradiation. Several p73 splice variants have been identified, including alpha (full-length), beta (missing exon 13), gamma (missing exon 11) and delta (missing exons 11, 12 and 13). Two hybrid analysis has shown variable interaction(s) between these isoforms in vitro. Many types of normal, tumor and virally-transformed cell lines express detectable levels of p73, however, the relative expression of p73 isoforms, as well as their functional activity, appears to be differentially regulated in various cell types. p73alpha and beta isoforms migrate at molecular weights of approximately 80 kDa (alpha) and 70 kDa (beta), respectively. The GC-15 antibody reacts with human p73alpha and beta. A fusion protein containing amino acids 380-367 of human p73alpha was used as immunogen.