GPR124 promotes cell migration.

Slides:

Advertisements

Similar presentations

Type VIIa1 collagen and laminin-γ2 promote a p53 mutant/HIF-1–dependent proinvasive phenotype. Type VIIa1 collagen and laminin-γ2 promote a p53 mutant/HIF-1–dependent.

Advertisements

Comparison (θ) of the mean dinucleotide variability distribution for (A) genes with MAE vs. Comparison (θ) of the mean dinucleotide variability distribution.

Comparison (R) of the mean observed to expected dinucleotide distribution for (A) genes with MAE vs. Comparison (R) of the mean observed to expected dinucleotide.

Balancing selection characterizes both MAE genes and cell type-specific genes (expressed in either nsc or asl but not in both). Balancing selection characterizes.

Posttranslational regulation of ETV5 and c-JUN in neurons.

Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25 cells. Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25.

CatL activity levels and expression of the DC forms of CatB and CatL are reduced in the α5β1-negative CHO cells. CatL activity levels and expression of.

FAM49B controls T cell activation by regulating cytoskeleton remodeling. FAM49B controls T cell activation by regulating cytoskeleton remodeling. (A) J.FAM49B.

Schematic representation of possible effects of different factors on systemic resilience. Schematic representation of possible effects of different factors.

Auxin and GA promote fruit growth by activating ABA catabolism in the early stage and are important for the regulation of interlinked regulatory loops.

DHEA(S) and Allo activated transcription factors NF-κB and CREB in serum-deprived PC12 cells. DHEA(S) and Allo activated transcription factors NF-κB and.

DHEA(S) and Allo induced the phosphorylation of PKC in serum-deprived PC12 cells. DHEA(S) and Allo induced the phosphorylation of PKC in serum-deprived.

Decreased cell polarity and adhesion protein expression after 56Fe radiation. Decreased cell polarity and adhesion protein expression after 56Fe radiation.

PGAM5 dephosphorylates ASK1.

H&E staining reveals defects in the CNS of Gpr124−/− mice.

HDAC3, but not HDAC2 is in complex with tau protein.

Pretreatment of VSV-GPΔ to form VSV-GP19K rescues infection in the α5β1-integrin-negative CHO cells. Pretreatment of VSV-GPΔ to form VSV-GP19K rescues.

Motor coordination is enhanced by genetic deletion of Best1 or MAOB but impaired by overexpression of MAOB. (A) Experimental timeline and schematic illustration.

Histological staining reveals glomeruloid-like bodies in the forebrain and spinal cord of Gpr124−/− mice. Histological staining reveals glomeruloid-like.

GPR124 expression in endothelial cells is responsible for the phenotypes observed in Gpr124−/− mice. GPR124 expression in endothelial cells is responsible.

PGAM5 is a protein Ser/Thr phosphatase that activates ASK1.

Despite a relatively small amount of PI3Kβ being associated with activated PDGFRs, it generates a more substantial proportion of the PIP3 that accumulates.

Phosphatase activity of PGAM5 is required for activation of ASK1.

PGAM5 associates with and activates ASK1.

Vegfa is overexpressed by E11

Pirh2 promotes p73 ubiquitination in vivo.

Long-term up-regulation of proliferative markers and down-regulation of cell migration factors along with increased intestinal metaplasia after 56Fe radiation.

(A) NK cell cytotoxicity assays against K562, H9, and Raji target cell lines in the presence (black) and absence (white) of an anti-NKp30 antibody, clone.

Transcriptional response to mating in whole A. gambiae females.

TME is dominant over the genotype in determining the epithelial architecture of TUM622 cells in vitro. TME is dominant over the genotype in determining.

CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells and suppress dysplasia. CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells.

Expression levels of the transgenic DIA1(R1204X) mutant in the inner ear of TG mice Expression levels of the transgenic DIA1(R1204X) mutant in the inner.

Absolute quantitation of class IA PI3K subunits and heterodimers in MEFs. (A) Immunoblot of endogenous p85α in lysates of MEFs (clones 1 or 2, genotypes.

Identification of the host interaction partners of HEV proteins in the human liver and fetal brain cDNA libraries. Identification of the host interaction.

Subcellular localization of HIS-24::GFP in his-24−/− mutant background after B. thuringiensis (BT) infection. Subcellular localization of HIS-24::GFP in.

A B CDK2 CDK2 inhibition P Activated KRAS P CP110 CP110

Immunofluorescece analysis of c-src and v-src distribution in wild-type yeast cells. Immunofluorescece analysis of c-src and v-src distribution in wild-type.

Detection and tracking of individual SNAP-tagged proteins on the surface of living cells. Detection and tracking of individual SNAP-tagged proteins on.

Immunoblot analysis of GpGCS1 expression in strains K41 (mating-type plus) and K34 (mating-type minus). Immunoblot analysis of GpGCS1 expression in strains.

Lymphocyte lineage trees produced by long-term live cell microscopy.

AKAP15 coimmunoprecipitates with CaV1

Association of endogenous cadherins with CDO and BOC

Expression of the mutants of HP1α and the mutant of SYCE2 in MCF7 cells or RPE cells. Expression of the mutants of HP1α and the mutant of SYCE2 in MCF7.

TRADD is recruited to the TLR4 signaling complex upon LPS stimulation.

ZFAND5 associates with 26S proteasomes and slows their migration in native PAGE. (A) Purified 26S proteasomes bind directly to ZFAND5. 26S proteasomes.

ZFAND5 expression is induced by dexamethasone, but not by heat shock or tunicamycin treatment. ZFAND5 expression is induced by dexamethasone, but not by.

CCR4 antagonists amplify immunogenicity of vaccines in vivo.

Activation of PKR by the PBM decoy peptide.

Proposed model of the tumor-suppressive effects of TPL2 in the lung.

Coupled folding equilibrium describing the shift toward denatured material upon interaction with the cellular interior, as formalized in Eqs. 3–5. Coupled.

BHLH1a localizes in the nucleus, and its overexpression alters rhythmic diel gene expression. bHLH1a localizes in the nucleus, and its overexpression alters.

Fig. 6. Effect of SAHA and ML on histone acetylation, BAX, and p21CDKN1A expression.PANC-1 and BxPC-3 cells were incubated for 48 hours with 5 µM.

Fig. 3. Rnd proteins induce stronger responses in subconfluent endothelial cells.HUVECs were transfected with Rnd1, Rnd2, Rnd3 or GFP-encoding plasmids.

Figure 2 Detection of atypical anti-neuronal antibodies Immunohistofluorescence assay on rat brain sagittal slices incubated with the patient's CSF and.

IL-6 inhibits insulin-induced formation of p85/IRS-1 complexes.

(A) Correlation between the shear modulus (Fig

Effect of overexpression of Gcs1p on mitochondrial morphology.

The P450scc construct increases functional P450scc expression resulting in elevated pregnenolone levels. The P450scc construct increases functional P450scc.

co-IP of LEDGF/p75 and MeCP2.

CDDO-Me induces apoptosis independent of Bcl-2 level as well as p53 status in human NSCLC cells. CDDO-Me induces apoptosis independent of Bcl-2 level as.

Enhancement of MYC-related HAT complex recruitment to the target genes and histone H4 acetylation by MAPJD. A, interaction of MAPJD with HAT complex containing.

Activation of multiple RTKs in chondrosarcoma cells.

Expression of CD40L and CD40 in human vascular atherosclerotic lesions in situ. Expression of CD40L and CD40 in human vascular atherosclerotic lesions.

ZTL interacts with CO and regulates its stability.

The interaction of PALB2 with BRCA1 is required for the assembly of PALB2, BRCA2, and RAD51 nuclear foci. The interaction of PALB2 with BRCA1 is required.

Effect of MIF siRNA on the production of MMP-13 induced by LPA

Fig. 3. Association between peak CTL019 expansion and response.

KDM4A levels affect the distribution of translation initiation factors

NSG2 interacts with AMPAR subunits GluA1 and GluA2.

D-GM3 promotes uPAR clustering on the cell surface and activates p38 MAPK. A, uPAR expression in cells was either knocked down by treatment with 4 independent.

Presentation transcript:

GPR124 promotes cell migration. GPR124 promotes cell migration. (A) Exogenous Flag-GPR124 is detected in bEnd3 or hCMEC brain endothelial cells by immunoblotting with anti-Flag antibodies. The total levels of GPR124 (endogenous plus exogenous) in bEnd3/GPR124 cells are about 2.6-fold higher than bEnd3 cells and similar to those in ECs of developing brain (Fig. S3J) (B) Overexpression of GPR124 enhanced migration in brain endothelial cells. n = 6, P < 0.001. Results are representative of three independent experiments. Mike Cullen et al. PNAS 2011;108:14:5759-5764 ©2011 by National Academy of Sciences