Fig. 4. Clinically defined SMN mutants show alterations in the association with telomerase complex proteins. Clinically defined SMN mutants show alterations.

Slides:

Advertisements

Similar presentations

Exogenous B56γ3 WT F395C WT F395C IgG Vinc Endogenous B56γ2,3 HA-IPInput Figure S1 HA-B56γ3 is unable to interact with endogenous B56γ. Lysates of U2OS.

Advertisements

Phosphorylation of serine 73 targets SREBP-1c for ubiquitination and proteasomal degradation Phosphorylation of serine 73 targets SREBP-1c for ubiquitination.

The Anaphase-Promoting Complex Regulates the Abundance of GLR-1 Glutamate Receptors in the Ventral Nerve Cord of C. elegans Peter Juo, Joshua M. Kaplan

Volume 23, Issue 3, Pages (February 2013)

Robert L.S Perry, Maura H Parker, Michael A Rudnicki Molecular Cell

Slicing-Independent RISC Activation Requires the Argonaute PAZ Domain

Lysine 63 Polyubiquitination of the Nerve Growth Factor Receptor TrkA Directs Internalization and Signaling Thangiah Geetha, Jianxiong Jiang, Marie W.

Volume 91, Issue 2, Pages (October 1997)

Volume 10, Issue 19, Pages (October 2000)

Fig. 3. Hts and Dlg are in a complex at the postsynaptic membrane of larval NMJs.(A–B″) PLA with HtsM and Dlg antibodies (green) performed on third instar.

Fig. 1. Chlamydia infection causes elevated levels of sortilin.

Fig. 2. Morphological changes of cultured adherent fibroblastic cells after OA treatment related to actin microfilament reorganization.(A) Cells observed.

Fig. 7. Motion adaptation increases time-dependent response modulations (TDRM) relatively to the average cell response.TDRM normalized to the value obtained.

A highly conserved six-amino-acid region in the C-terminal CT domain of MARCH8 is responsible for its ability to downregulate TfR. A highly conserved six-amino-acid.

Fig. 2. p85β regulates cell adhesion

Fig. 7. Knockdown of Meis1 abolishes CR4. 2-GFP expression

The effects of a dominant negative mutant of lamin B1 on lamin distribution in HeLa cells. The effects of a dominant negative mutant of lamin B1 on lamin.

Fig. 2. Mapping of the interaction domain on coilin for association with the dyskerin complex. Mapping of the interaction domain on coilin for association.

Fig. 1. Exogenous folic acid and Folr1 rescues the function of a Rho-kinase binding mutation in Shroom3. Exogenous folic acid and Folr1 rescues thefunction.

Fig. 5. Expression of either dFMRP or human FMRP does not induce eIF2α phosphorylation.(A) Analysis of eIF2α phosphorylation upon dFMRP expression. Expression.

TP53 western blot of primary cultured tail cells from both wild-type (WT) and Tp53Δ11/Δ11 (−/−) rats. TP53 western blot of primary cultured tail cells.

Fig. 4. The model of malate metabolism in fruit cells under different K level conditions. The model of malate metabolism in fruit cells under different.

Fig. 1. Coilin interaction with the telomerase complex protein dyskerin is mediated by hTR. Coilin interaction with the telomerase complex protein dyskerin.

Table 2. Cell surface abundance of β1 integrin measured by flow cytometry.DDR wild type and DDR over-expressing cells were treated with deoxymannojirimycin.

Abraxas binds to BRCT–PALB2(L21P) and is involved in the recruitment of this fusion protein or of endogenous PALB2 to sites of DNA damage. Abraxas binds.

Fig. 2. DDR1 over-expression enhances collagen fibril reorganization

Fig. 3. Mutation of Y520 and Y667 result in increased delivery of prestin to the apical surface of MDCK cells.MDCK cells transiently transfected with wt.

Fig. 7. A model for the negative regulation of SMN and coilin on telomerase biogenesis. A model for the negative regulation of SMN and coilin on telomerase.

Fig. 3. Coilin levels correlate with altered nascent U2 snRNA, hTR and rRNA levels.RNA isolated from HeLa or WI-38 cells following RNAi targeting coilin.

Fig. 3. The checkpoint proteins Mad2 and BubR1 remain associated with the kinetochores of unaligned chromosomes in cenp-metaΔ mutant cells entering anaphase.(A–C)

Fig. 5. GFP fluorescence colocalization of Gcn5.

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. 6. Coilin mutants display differential hTR processing activity but lack specificity toward the 5′ or 3′ regions.(A) Illustration of human telomerase.

Fig. 4. One-dimensional gel electrophoresis of DIMs

Fig. 2. Pull down of CaV2. 2 by channel C terminal fusion protein

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

Fig. 4. Coilin phosphomutant displays differential RNA binding and degradation activities.Purified proteins were analyzed for RNase activity with total.

Fig. 7. Ror-GFP binds to Myc-tagged Wnts and Wnt receptors.

Fig. 1. Mitotic arrest results in differential RNA association with coilin.Untreated or nocodazole treated HeLa cell lysate was used for RNA immunoprecipitations.

Figure 4 DNM1 mutations affect protein levels and self-dimerization (A) HeLa cells were transfected with green fluorescent protein (GFP)-tagged mutant.

RXRa serves as a carrier for TR3 translocation initiated by 9-cis retinoic acid. RXRa serves as a carrier for TR3 translocation initiated by 9-cis retinoic.

Fig. 8. The morphology of the ventral nerve cord in Ror-Myc overexpressing embryos is normal. The morphology of the ventral nerve cord in Ror-Myc overexpressing.

Reb does not play a significant role in regulating TGF-β signaling

Fig. 3. Overexpression of wild-type GFP-CPAP, but not GFP-CPAP-377EE (GFP-377EE), induces cilia formation and promotes the growth of cilia.CAD cells (A,B)

ArfGAP1 expression alters GBF1 recruitment to Golgi membranes.

The SIM domain of RAD51 is required for HR

Expression of active Rho partially rescues Erk1/2 activation and peripheral FA phenotype in RIAM-knockdown cells. Expression of active Rho partially rescues.

Lysine residues in the cytoplasmic region of TfR are involved in the MARCH8-induced downregulation of TfR. Lysine residues in the cytoplasmic region of.

Effect of the siRNA-mediated knockdown of endogenous MARCH8 on the expression levels of MARCH8 substrates, TfR and CD98, in HepG2 cells. Effect of the.

Fig. 2. Coupling of actin to cell–cell junctions requires α-catenin and is necessary for the establishment of the barrier.(A) Effect of Cytochalasin D.

Fig. 4. CR4.2 may be active in amacrine cells but not in ganglion cells.Chick retinas were electroporated with either the control CAG-GFP construct or.

Volume 16, Issue 16, Pages (August 2006)

BRG1 interacts with RAD52 and regulates its accumulation at DSB sites during homologous recombination repair. BRG1 interacts with RAD52 and regulates its.

Fig. 2. Acetylation stiffens primary cilia.

Fig. 8. Compared mobilities of passenger proteins in G2/M-prophase, metaphase and anaphase.FRAP experiments were performed on HeLa cells stably expressing.

Fig. 1. Rnd2 and Rnd3 induce stress fibres whereas Rnd1 reduces stress fibres in endothelial cells.(A) Rnd mRNAs are expressed in HUVECs. Total RNA was.

Fig. 6. RhoB is required for Rnd3-induced stress fibre formation

Fig. 6. Bj mutants show stereocilia patterning defects and biliary duct (BD) malformations. Bj mutants show stereocilia patterning defects and biliary.

Fig. 5. Co-expression analyses of disease mutations in YFP-RPGRIP1α1 with wild-type RFP-RPGR1–19 or RFP-RPGRORF15 in COS7 cells.YFP-RPGRIP1α1 with disease-associated.

WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates TfR. WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates.

Fig. 4. Tetracycline-regulated expression of ClC-5 in the HEK293 cells stably expressing gastric H+,K+-ATPase.(A) Alignments of rat ClC-5, human ClC-5,

Fig. 3. Inclusion of E-cadherin into stationary clusters requires cis-, trans-, and cytoplasmic interactions. Inclusion of E-cadherin into stationary clusters.

Phenotypic analysis of the CNS in mutants for Ror, otk and otk2

Fig. 7. Analysis of dFMRP kinetics in dFMRP granules by FRAP

Dynamics of actin-binding proteins in the ICAM-1 complex.

Vps36 interacts with Smo in the absence of Hh

GOLPH3 interacts with COG complex proteins.

Mutant MFN2 proteins have normal half-lives and are properly localized to mitochondria. Mutant MFN2 proteins have normal half-lives and are properly localized.

Fig. 6 The C9ORF72/SMCR8 complex regulates ULK1.

The interaction between PARsylated BRCA1 and RAP80 is required for maintaining BRCA1–RAP80–PARP1 complex integrity after DNA damage and normal HRR regulation.

Presentation transcript:

Fig. 4. Clinically defined SMN mutants show alterations in the association with telomerase complex proteins. Clinically defined SMN mutants show alterations in the association with telomerase complex proteins. (A-B) Cells were transfected with wild-type (WT) or clinically defined SMN mutations, fused to GFP. IPs were performed using anti-GFP antibody. The resulting immunocomplexes were then probed for either dyskerin (A) or NAF1 (B). (C) Graphical representation of the data shown in (A) and (B) (n=8), normalized to the recovery of dyskerin and NAF1 by WT SMN. *P<0.05 compared to WT SMN, which serves as a control. Error bars represent standard error about the mean. For all IPs, inputs represent 1.5% the amount of the lysate used in the IP reaction. Note that GFP vector alone does not recover significant amounts of dyskerin (Fig. 2B, lane 5). Aaron R. Poole, and Michael D. Hebert Biology Open 2016;bio.018804 © 2016. Published by The Company of Biologists Ltd