FLIP anticorps (AA 1-480)
Aperçu rapide pour FLIP anticorps (AA 1-480) (ABIN1169018)
Antigène
Voir toutes FLIP (CFLAR) AnticorpsReactivité
Hôte
Clonalité
Conjugué
Application
Clone
-
-
Épitope
- AA 1-480
-
Specificité
- Recognizes short (FLIPS) and long (FLIPL) splice variants of human FLIP. This antibody recognizes an epitope in the N-terminal DED region (aa1-194).
-
Réactivité croisée
- Humain
-
Purification
- Purified from concentrated hybridoma tissue culture supernatant.
-
Immunogène
- Recombinant human FLIP (aa 1-480).
-
Isotype
- IgG1
-
-
-
-
Indications d'application
- Optimal working dilution should be determined by the investigator.
-
Restrictions
- For Research Use only
-
-
-
Format
- Liquid
-
Concentration
- Lot specific
-
Buffer
- In PBS containing 10 % glycerol and 0.02 % sodium azide.
-
Agent conservateur
- Sodium azide
-
Précaution d'utilisation
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
-
Stock
- 4 °C,-20 °C
-
Stockage commentaire
-
Short Term Storage: +4°C
Long Term Storage: -20°C
Stable for at least 1 year after receipt when stored at -20°C. -
Date de péremption
- 12 months
-
-
-
: "The TRAIL-Induced Cancer Secretome Promotes a Tumor-Supportive Immune Microenvironment via CCR2." dans: Molecular cell, Vol. 65, Issue 4, pp. 730-742.e5, (2017) (PubMed).
: "The c-FLIP-NH2 terminus (p22-FLIP) induces NF-kappaB activation." dans: The Journal of experimental medicine, Vol. 203, Issue 5, pp. 1295-305, (2006) (PubMed).
: "Suramin inhibits death receptor-induced apoptosis in vitro and fulminant apoptotic liver damage in mice." dans: Nature medicine, Vol. 10, Issue 6, pp. 602-9, (2004) (PubMed).
: "Lack of proapoptotic activity of soluble CD95 ligand is due to its failure to induce CD95 oligomers." dans: Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, Vol. 23, Issue 8, pp. 441-7, (2003) (PubMed).
: "Proteasome inhibition results in TRAIL sensitization of primary keratinocytes by removing the resistance-mediating block of effector caspase maturation." dans: Molecular and cellular biology, Vol. 23, Issue 3, pp. 777-90, (2003) (PubMed).
: "An inducible pathway for degradation of FLIP protein sensitizes tumor cells to TRAIL-induced apoptosis." dans: The Journal of biological chemistry, Vol. 277, Issue 25, pp. 22320-9, (2002) (PubMed).
: "Enhancement of Apo2L/TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)-induced apoptosis in non-small cell lung cancer cell lines by chemotherapeutic agents without correlation to the ..." dans: The Journal of thoracic and cardiovascular surgery, Vol. 123, Issue 1, pp. 168-74, (2002) (PubMed).
: "Caspase-10 is recruited to and activated at the native TRAIL and CD95 death-inducing signalling complexes in a FADD-dependent manner but can not functionally substitute caspase-8." dans: The EMBO journal, Vol. 21, Issue 17, pp. 4520-30, (2002) (PubMed).
: "The role of c-FLIP in modulation of CD95-induced apoptosis." dans: The Journal of biological chemistry, Vol. 274, Issue 3, pp. 1541-8, (1999) (PubMed).
-
-
- FLIP (CFLAR) (CASP8 and FADD-Like Apoptosis Regulator (CFLAR))
-
Autre désignation
- FLIP
-
Sujet
- FLIP is an apoptosis regulator protein which functions as a crucial link between cell survival and cell death pathways in mammalian cells and acts as an inhibitor of TNFRSF6 mediated apoptosis. A proteolytic fragment (p43) is likely retained in the death-inducing signaling complex (DISC) thereby blocking further recruitment and processing of caspase-8 at the complex. Full length and shorter isoforms have been shown either to induce apoptosis or to reduce TNFRSF-triggered apoptosis. FLIP lacks enzymatic (caspase) activity. FLIP is highly expressed in skeletal muscle, pancreas, heart, kidney, placenta and peripheral blood leukocytes.
-
UniProt
- O15519
-
Pathways
- Apoptose, Regulation of Muscle Cell Differentiation, Skeletal Muscle Fiber Development
Antigène
-