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1.
Fig. 4.

Fig. 4. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Neurotrophin-independent signaling to NRIF and TRAF6 by disulfide-crosslinked p75NTR mutants. (A,B) Binding of NRIF to wild-type and mutant p75NTR in transfected HEK293 cells. (C,D) Binding of TRAF6 to wild-type and mutant p75NTR in transfected HEK293 cells.

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.
2.
Fig. 5.

Fig. 5. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Neurotrophin-independent signaling to JNK and caspase-3 by disulfide-crosslinked p75NTR mutants. (A) Phosphorylation of JNK in HEK293 cells transfected with vector or p75NTR constructs in the presence of sortilin. Results are expressed as average of triplicate measurements ± s.d. *P<0.05 vs wild type without proBDNF; n=3. (B) Activation of caspase-3 in HEK293 cells transfected with vector or p75NTR constructs in the presence of sortilin. Results are expressed as average of triplicate measurements ± s.d. *P<0.05 vs wild type without proBDNF; n=3. (C) Phosphorylation of JNK in HEK293 cells transfected with vector or p75NTR constructs in the presence of sortilin. (D) Activation of caspase-3 in HEK293 cells transfected with vector or p75NTR constructs in the presence of sortilin. Arrows denote cleaved caspase-3.

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.
3.
Fig. 3.

Fig. 3. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Neurotrophin-independent signaling to RIP2 and NF-κB by disulfide-crosslinked p75NTR mutants. (A) Binding of RIP2 to wild-type and mutant p75NTR in transfected COS cells assayed by immunoprecipitation (IP) and immunoblotting (IB). (B) NF-κB activity in native and transfected cerebellar granule cells. Results are expressed as average of triplicate measurements ± s.d. *P<0.05 vs control (i.e. without NGF or exogenous p75NTR); n=3. (C) NF-κB activity in transfected M23 fibroblast cells. Results are expressed as average of triplicate measurements ± s.d. *P<0.05 vs wt without NGF; n=3.

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.
4.
Fig. 6.

Fig. 6. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Disulfide-crosslinked p75NTR mutants do not mimic the activities of myelin ligands MAG and Nogo. (A) Binding of RhoGDI to wild-type p75NTR and T249C mutant in COS cells cotransfected with NgR and Lingo-1 and stimulated with MAG-Fc (top) or Nogo-66 peptide (bottom). Similar results were observed in two additional experiments. (B) RhoA activity in COS cells transfected with wild-type p75NTR and the indicated mutants in the presence of NgR and Lingo-1 following stimulation with MAG-Fc. Results are expressed as mean ± s.d. relative to wt without MAG treatment. *P<0.05 vs control; n=3.

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.
5.
Fig. 1.

Fig. 1. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Disulfide-linked dimers of p75NTR. (A) Cysteine-scanning mutagenesis in the juxtamembrane region of the p75NTR extracellular domain. (B) Cell-surface expression of disulfide-linked p75NTR dimers (dim) and monomers (mon) in transfected COS cells visualized by Neutravidin probing of p75NTR immunoprecipitates under nonreducing (–DTT) and reducing (+DTT) conditions. Note that, in nonreducing conditions, p75NTR dimers run somewhat higher, and monomers lower, than their predicted molecular masses. Results are expressed as average percentage of surface receptor present in the disulfide-linked dimer form ± s.d. of three independent determinations.

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.
6.
Fig. 2.

Fig. 2. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Disulfide-crosslinked p75NTR mutants display normal NGF binding and intramembrane proteolysis. (A) Binding of 125I-NGF to wild-type and mutant p75NTR analyzed by chemical crosslinking. Samples were run under reducing conditions. For each construct, binding counts were normalized to levels of expression as assessed by immunoblotting (IB). Results are expressed as average ± s.d. of three independent determinations. (B) Intramembrane cleavage of wild-type and and mutant p75NTR following stimulation with PMA in transfected COS cells. The proteasome inhibitor epoxomycin was used to prevent degradation of CTF and ICD fragments. Mutant and wild-type (wt) p75NTR molecules were visualized by immunoblotting. CTF, C-terminal fragment; ICD, intracellular domain. The histogram plots the ratio between ICD and full-length p75NTR constructs expressed as average ± s.d. of three independent experiments.

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.
7.
Fig. 8.

Fig. 8. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Disulfide-linked p75NTR mutants induce cell death in vitro and in vivo. (A) Cell death assayed by TUNEL 24 hours after addition of proBDNF in HEK293 cells transfected with p75NTR constructs and sortilin as indicated. Results are expressed as mean ± s.d. of three independent experiments, each performed in duplicate. *P<0.05 vs wt. (B) Expression of p75NTR constructs (HA immunohistochemistry, green) and activated caspase-3 (red) in electroporated chick neural tubes. (C) Analysis of cell death by activated caspase-3 staining in electroporated chick neural tubes. Results are expressed as the difference between electroporated and control sides in the number of active caspase-3-positive cells per section ± s.e.m. (n=4-6 embryos, 20-22 sections were analyzed per embryo).

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.
8.
Fig. 7.

Fig. 7. From: Ligand-independent signaling by disulfide-crosslinked dimers of the p75 neurotrophin receptor.

Constitutive axonal retrograde transport of disulfide-linked p75NTR mutants. (A) Five individual frames from a confocal time series of a motoneuron axon displaying the kinetics of transport of HA-tagged wild-type p75NTR before and after NGF treatment. Arrowheads indicate p75NTR-containing vesicles. Corresponding phase or DIC images are shown below. The retrograde direction is indicated by the arrow on top. Scale bar: 10 μm. (B) Representative displacement graphs of axonal retrograde carriers containing wild-type and p75NTR mutants in the presence and absence of NGF. (C) Quantitative analysis of axonal retrograde transport (carriers per minute) for wild-type and mutant p75NTR constructs. Results are expressed as mean ± s.e.m. of 3-5 independent experiments. Each independent experiment consisted in the analysis of at least three axons. ***P<0.001 vs control; **P<0.01 vs control; *P<0.05 vs wt.

Marçal Vilar, et al. J Cell Sci. 2009 September 15;122(18):3351-3357.

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