Work with LifeSpan to design a custom immunohistochemistry to address your specific biological question. Outsource the entire localization process without having to
worry about finding and characterizing target specific antibodies, sourcing and validating difficult-to-find tissues, and having the ability to interpret the resulting
immunostaining in relation to complex human pathologies.
Test your therapeutic antibodies in immunohistochemistry against a broad panel of normal frozen human tissue types in order to determine potential unintended binding.
Our non-GLP TCR services are designed on the FDA recommendation outlined in their "Points to Consider in the Manufacture and Testing of Monoclonal Antibody Products for Human Use".
LS-F39120 is a 96-well enzyme-linked immunosorbent assay (ELISA) for the Quantitative detection of Human TCF7L2 / TCG4 in samples of Cell Lysates and Tissue Homogenates. It is based upon a Sandwich assay principle and can be used to detect levels of TCF7L2 / TCG4 as low as 0.054 nanograms per millilter.
Due to their limited shelf life, LSBio ELISA kits are not typically stocked as finished goods. Upon receipt of an order each kit is assembled and tested to ensure that it meets specifications before shipping. Minor changes may occur to the Range, Sensitivity, and Precision. In the event of a significant change the order would be confirmed with the customer before shipping ELISA kit lot numbers reflect the date of final assembly and testing for each specific kit rather than a bulk manufactured lot. All kits are tested to confirm that they fall within their defined Inter- and Intra- assay coefficient of variation.
Participates in the Wnt signaling pathway and modulates MYC expression by binding to its promoter in a sequence-specific manner. Acts as repressor in the absence of CTNNB1, and as activator in its presence. Activates transcription from promoters with several copies of the Tcf motif 5'-CCTTTGATC-3' in the presence of CTNNB1. TLE1, TLE2, TLE3 and TLE4 repress transactivation mediated by TCF7L2/TCF4 and CTNNB1. Expression of dominant-negative mutants results in cell-cycle arrest in G1.