Anti-Mouse TIM-1 (CD365) - Purified in vivo PLATINUM™ Functional Grade

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TIM-1 is a member of the T cell immunoglobulin mucin gene family and encodes a cell-surface
glycoprotein consisting of an immunoglobulin variable-region-like domain (IgV), mucin-like
domain, transmembrane domain, and intracellular tail1, 2. TIM-1 promotes activated T cell
survival and plays a role in immunopathology2. TIM-1 is also expressed by tubules injured by
renal disease and in this context is known by its alternative name, kidney injury molecule-1
(KIM-1). Renal expression of TIM-1 is associated with dedifferentiation of epithelial cells and is
involved in the phagocytosis of apoptotic debris. TIM-1 also plays a role in immune responses
and is linked to airway hypersensitivity in mice and asthma, eczema, and rheumatoid arthritis in
humans1. TIM-1 was first identified as a hepatitis A virus cellular receptor1. TIM-4 is a natural
ligand of TIM-1.
RMT1-10 was generated by immunizing SD rats with full-length TIM-1-Ig containing both the
IgV and mucin domains1. Lymph nodes were fused with P3U1 myeloma cells. Resulting
hybridomas were screened for binding to mouse TIM-1-transfected CHO cells.
RMT1-10 binds to full-length and mucinless forms of TIM-1, suggesting its epitope resides in
the IgV domain1. Blocking TIM-1 in culture via the addition of RMT1-10 results in reduced T
cell proliferation, IFN-γ and IL-17 inhibition, and induction of the Th2 cytokines IL-4 and IL-101. Additionally, RMT1-10 significantly improves the survival rate of corneal allografts3, 4 and
attenuates atherosclerosis development and progression by expanding atheroprotective B1a cells5 in mice.

This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.