Anti-Tob (4B1) Mouse IgG MoAb

Catalogue Number: 10031-IBL

Manufacturer:IBL - (Immuno-Biologicals Laboratories Co Ltd)
Physical state:Lyophilized product from 1 % BSA in PBS containing 0.05 % NaN3
Type:Monoclonal Primary Antibody - Unconjugated
Shipping Condition:Blue Ice
Storage Condition:2-8°C
Unit(s): 200 ug, 10 ug
Host name:
Clone: 4B1
Isotype: IgG2a
Immunogen: Recombinant Tob


Description: A cDNA for a novel protein termed Tob (Transducer of ErbB-2) that interacts with the c-erbB-2 gene product p185erbB2 was molecularly cloned. Nucleotide sequencing reveals that the Tob protein is a 45 kDa protein that does not contain either SH2 or SH3 domain but is homologous to the previously characterized anti-proliferative gene product BTG-1 at its amino-terminal half. The carboxyl-terminal half of Tob is characterized by the presence of a sequence rich in proline and glutamine and shows no homology to known proteins. Like BTG-1, exogenously expressed Tob is able to suppress growth of NIH3T3 cells, but the growth suppression is hampered by the presence of kinase-active p185erbB2. By using the SGT-Tob protein that contains either full length or amino-terminal half of Tob, The carboxyl-terminal half of Tob is relevant to its interaction with p185erbB2. In addition, co-immunoprecipitation of the Tob protein with anti-ErbB-2 antibody and reciprocally the p185erbB2 with anti-Tob antibodies could be conducted. These data suggest that p185erbB2 negatively regulates the Tob-mediated anti-proliferative pathway through its interaction with Tob, requlsing possibly in growth stimulation by p185erbB2. The expression of the Tob mRNA is observed in various cell types and is not correlated with expression of c-erbB-2, suggesting that other receptor-type protein-tyrosine kinases are also involved the Tob-mediated regulation of cell growth. Tob is a member of an emerging family of genes with anti-proliferative function. Tob is rapidly phosphorylated at Ser 152, Ser 154, and Ser 164 by Erk1 and Erk2 upon growth-factor stimulation. Tob inhibits cell growth by suppressing cyclin D1 expression, which is canceled by Erk1- and Erk2-mediated Tob phosphorylation. In recent, it is reported that mutant forms of Tob, in which serines are replaced by glutamic acids to mimic phosphorylation, show a much reduced ability to inhibit the cell cycle progression to S phase from G0/G1 phase, as compared with wild-type Tob, indicating that ERK phosphorylation negatively regulates the anti-proliferative function of Tob.


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