Inhibition of p38 mitogen-activated protein kinase reduces TNF-induced activation of NF-kappaB, elicits caspase activity, and enhances cytotoxicitymore suppliers
In Molecular Cancer, 2003
... Antibodies against phospho-JNK, JNK, phospho-p38, phospho-CREB, CREB, and c-FLIPL were from Cell Signaling Technology (Beverly, MA, USA) ...
Biology and oncogenicity of the Kaposi sarcoma herpesvirus K1 protein.
Botucatu, Brazil. In Rev Med Virol, Sep 2015
KSHV is unique among other human herpesviruses because of the elevated number of viral products that mimic human cellular proteins, such as a viral cyclin, a viral G protein-coupled receptor, anti-apoptotic proteins (e.g., v-bcl2 and v-FLIP), viral interferon regulatory factors, and CC chemokine viral homologues.
Lesser-Known Molecules in Ovarian Carcinogenesis.
Jászvásár, Romania. In Biomed Res Int, 2014
Within this framework, this review presents three protein molecules: ALCAM, c-FLIP, and caveolin, motivated by the perspectives provided through the current limited knowledge on their role in ovarian carcinogenesis and on their potential as prognosis factors.
The Accomplices of NF-κB Lead to Radioresistance.
Beijing, China. In Curr Protein Pept Sci, 2014
Moreover, we describe how the expression of the target genes (e.g., XIAP, A20, FLIP, Bcl-xL) are induced by NF-κB to regulate the activation of survival signaling pathways and to inhibit apoptotic signaling pathways.
A long-awaited merger of the pathways mediating host defence and programmed cell death.
More papers using
New York City, United States. In Nat Rev Immunol, 2014
Molecules such as receptor-interacting protein kinase 1 (RIPK1), RIPK3, FAS-associated death domain protein (FADD), FLICE-like inhibitory protein (FLIP) and caspase 8 - which are associated with different forms of cell death - are incorporated into compatible and exceedingly dynamic Toll-like receptor, NOD-like receptor and RIG-I-like receptor signalling modules.