Granzyme B Inhibitor I, The Granzyme B Inhibitor I controls the biological activity of Granzyme B. This small molecule/inhibitor is primarily used for Cancer applications.
A weak inhibitor of the human and murine granzyme B. Also inhibits the apoptosis-related DNA fragmentation in lymphocytes by fragmentin 2, a rat lymphocyte granule protease homologous to granzyme B (ID50 = 300 nM).
A weak inhibitor of the human and murine serine protease granzyme B. Also inhibits the apoptosis related DNA fragmentation in lymphocytes by fragmentin 2, a rat lymphocyte granule protease homologous to granzyme B (ID50 = 300 nM).
Acciones bioquímicas o fisiológicas
Cell permeable: yes
Primary Target Granzyme B
Product does not compete with ATP.
Reversible: no
Target IC50: 300 nM against the apoptosis-related DNA fragmentation in lymphocytes by fragmentin 2
Advertencia
Toxicity: Standard Handling (A)
Secuencia
Z-Ala-Ala-Asp-CH₂Cl
Reconstitución
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.
Otras notas
Gong, B., et al. 1999. Cell Growth Different. 10, 491. Shi, L., et al. 1992. J. Exp. Med. 176, 1521. Odake, S., et al. 1991. Biochemistry30, 2217.
Información legal
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Código de clase de almacenamiento
11 - Combustible Solids
Clase de riesgo para el agua (WGK)
WGK 1
Punto de inflamabilidad (°F)
Not applicable
Punto de inflamabilidad (°C)
Not applicable
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Frontiers in neurology, 10, 1306-1306 (2020-01-11)
Hippocampal neuronal apoptosis is a devastating consequence of cardiac arrest (CA) and subsequent cardiopulmonary resuscitation (CPR). In this study, we assessed the contribution of cytotoxic T lymphocyte (CTL)-derived toxic mediator granzyme B (Gra-b) to the hippocampal neuronal apoptosis following CA/CPR
Penetration of immune cells into tumor cells was believed to be immune-suppressive via cell-in-cell (CIC) mediated death of the internalized immune cells. We unexpectedly found that CIC formation largely led to the death of the host tumor cells, but not
Infiltration of leukocytes into post-ischemic cerebrum is a well-described phenomenon in stroke injury. Because CD-8(+) T-lymphocytes secrete cytotoxic proteases, including granzyme-b (Gra-b) that exacerbates post-ischemic brain damage, we investigated roles of Gra-b in human stroke. To study the role of
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