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.
TCR Screening Services
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".
BAD Antibody, BBC2 Antibody, Bcl-2-like protein 8 Antibody, BCL2-binding component 6 Antibody, BCL2L8 Antibody, BBC6 Antibody, BCL-X/BCL-2 binding protein Antibody, Bcl-2-binding component 6 Antibody, Bcl2 antagonist of cell death Antibody, BCL2-binding protein Antibody, Bcl2-L-8 Antibody
Members in the Bcl-2 family are critical regulators of apoptosis by either inhibiting or promoting cell death. Bcl-2 homology 3 (BH3) domain containing pro-apoptotic proteins, such as Bax, Bid, and Bik, form a growing subclass of the Bcl-2 family. Another such protein is the Bcl-2-antagonist of cell death (Bad). Bad regulates apoptosis by forming heterodimers with anti-apoptotic proteins Bcl-2 and Bcl-xL, thereby preventing them from binding with Bax.
Immunofluorescence microscopy of BAD using LS-C148207 at 1:2000. Du145 human prostate carcinoma cells were cultured without (A) or with (B and C) 1 uM of the triphosphatase inhibitor thapsigargin (THG) for 12 hr. A and B, staining with BAD antibody, followed by a FITC-conjugated secondary antibody. C, staining with a mitochondrial marker (antibody to mitochondrial Hsp60), followed by a rhodamine-conjugated secondary antibody. THG induces Ca2+ release from internal stores which can promote apoptosis. BAD staining was located diffusely throughout the cytoplasm of untreated cells (A), and localized to the mitochondria in treated cells (B).
Requested From: United States
Date Requested: 10/24/2016