The SIM domain of RAD51 is required for HR

Slides:



Advertisements
Similar presentations
JNK is activated by Wnt5a.
Advertisements

Expression of SYCE2 activates the DSB repair pathway.
Aggregation is not required for cytoplasmic relocalization induced by misfolding mutations. Aggregation is not required for cytoplasmic relocalization.
Fig. 4. Clinically defined SMN mutants show alterations in the association with telomerase complex proteins. Clinically defined SMN mutants show alterations.
VacA does not induce phosphorylation of Src in RPTPα constitutive-knockdown AZ-521 cells. VacA does not induce phosphorylation of Src in RPTPα constitutive-knockdown.
RNAi screen for host factors involved in L. monocytogenes dissemination. RNAi screen for host factors involved in L. monocytogenes dissemination. (A) Images.
BTN1 mRNA level in response to extracellular pH determined by comparative RT2PCR. BTN1mRNA level in response to extracellular pH determined by comparative.
Fig. 2. Morphological changes of cultured adherent fibroblastic cells after OA treatment related to actin microfilament reorganization.(A) Cells observed.
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.
A Drosophila cell culture model to study VAP(P58S) aggregation.
The C-terminal membrane-proximal region of MARCH8 interacts with TfR.
Fig. 5. Expression of either dFMRP or human FMRP does not induce eIF2α phosphorylation.(A) Analysis of eIF2α phosphorylation upon dFMRP expression. Expression.
IQGAP3 is a novel member of the IQGAP family.
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.
Directed differentiation of hPSCs to hypothalamic progenitors.
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.
The initial targeting of Sec61b mRNA to the ER is partially dependent on ribosomes and translation. The initial targeting of Sec61b mRNA to the ER is partially.
Fcp1 CTD phosphatase affects a broad range of transcripts in the +N and -N media. Fcp1 CTD phosphatase affects a broad range of transcripts in the +N and.
Fusion of PALB2 to the BRCT repeats of BRCA1 mediates the assembly of DNA damage foci by PALB2 and RAD51 in BRCA1-deficient cells. Fusion of PALB2 to the.
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.
FAK tyrosine phosphorylation is unaffected by loss of LAR activity.
High-affinity binding to the hypervariable region of the β1 I-like domain controls signaling to fibronectin fibrillogenesis. High-affinity binding to the.
Fig. 3. Rnd proteins induce stronger responses in subconfluent endothelial cells.HUVECs were transfected with Rnd1, Rnd2, Rnd3 or GFP-encoding plasmids.
Sox2 and Isl1 cooperate to orchestrate Merkel cell differentiation.
Fig. 1. Mitotic arrest results in differential RNA association with coilin.Untreated or nocodazole treated HeLa cell lysate was used for RNA immunoprecipitations.
Fusion of PALB2(L21P) to the BRCT repeats of BRCA1 mediates the assembly of DNA damage foci by PALB2 and RAD51 in PALB2-deficient cells. Fusion of PALB2(L21P)
Figure 4 DNM1 mutations affect protein levels and self-dimerization (A) HeLa cells were transfected with green fluorescent protein (GFP)-tagged mutant.
ArfGAP1 expression alters GBF1 recruitment to Golgi membranes.
Reconstitution of GBF1 recruitment to Golgi membranes in a cell-free assay. Reconstitution of GBF1 recruitment to Golgi membranes in a cell-free assay.
Effect of Dipy on the expression of chondrogenic markers.
The K86M mutation in ABCG2 results in a non-functional transporter.
ABCG2-K86M shows a markedly reduced surface expression.
dcn1-deletion results in attenuated cohesin cleavage at anaphase
Defective MEK-Erk1/2 kinase activation in RIAM-depleted cells accounts for their impaired FA disassembly. Defective MEK-Erk1/2 kinase activation in RIAM-depleted.
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.
The expression of two forms of N-cadherin.
RAD51 interacts with SUMO-1 through its SIM
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.
Kinetics of GFP secretion from CHO cells.
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.
Loss of Graf results in plasmatocyte overproliferation.
BRG1 interacts with RAD52 and regulates its accumulation at DSB sites during homologous recombination repair. BRG1 interacts with RAD52 and regulates its.
Peroxisome speeds were slower in patient and control cells.
Misfolding mutations impair the BRCA1 nuclear aggregation in yeast and the BRCA1 nuclear localization in human cells. Misfolding mutations impair the BRCA1.
Depletion of COPI protein inhibits cis to trans cisternal maturation.
Integrins are required to strengthen Notch signaling.
The lmpA kd strain shows severe defects in phagocytosis.
Integrins modulate the Notch pathway by regulating its intracellular trafficking and/or processing. Integrins modulate the Notch pathway by regulating.
EPLIN also plays a crucial role in the apical extrusion of RasV12-transformed cells. EPLIN also plays a crucial role in the apical extrusion of RasV12-transformed.
PtdIns(4,5)P2 dependence of TbEpsinR and TbCALM membrane targeting.
WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates TfR. WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates.
Ub-binding ability of ERα.
Lack of Ctip2 is associated with impaired proliferation and delayed onset of differentiation during early stages of epidermal development. Lack of Ctip2.
p65 depletion increases basal protein aggregation and insolubilization
Telomere cohesion is established in S phase in cohesin-ring-depleted cells. Telomere cohesion is established in S phase in cohesin-ring-depleted cells.
Vps36 interacts with Smo in the absence of Hh
Role of Src and PTP-PEST in upregulation of tyrosine phosphorylation of paxillin and FAK. (A) Mock and D11 cells were pre-incubated with PP2 or PP3 (10 µM,
Generation of an inducible form of FOXN1.
GOLPH3 interacts with COG complex proteins.
Ctip2 directly regulates Notch1 expression in differentiated cells.
Expedited loss of MacroH2A
Overexpression of GFP-fused PH domain of Gcs1p did not affect distribution of mitochondrial or ER markers or actin. Overexpression of GFP-fused PH domain.
The role of FOXN1 in initiation of terminal differentiation.
4-OHE2 induces neoplastic cell transformation and PCNA expression.
Fig. 4 Dcr-2 binds to the 3′UTR of Toll mRNA.
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.
BRCA1 sequence variants classified as pathogenic do not restore HR
KDM4A levels affect the distribution of translation initiation factors
Presentation transcript:

The SIM domain of RAD51 is required for HR The SIM domain of RAD51 is required for HR. (A) HR activity of RAD51-depleted cells (siRAD51), expressing NLS (vector), NLS-RAD51-WT, NLS-RAD51-V2645K or NLS-RAD51-AAAS, was analyzed using the DR-GFP assay. The SIM domain of RAD51 is required for HR. (A) HR activity of RAD51-depleted cells (siRAD51), expressing NLS (vector), NLS-RAD51-WT, NLS-RAD51-V2645K or NLS-RAD51-AAAS, was analyzed using the DR-GFP assay. Columns represent the mean of the proportions of GFP-positive cells from four independent experiments. Error bars represent s.d. (B) Expression of NLS-RAD51-WT, NLS-RAD51-V2645K or NLS-RAD51-AAAS in RAD51-depleted cells (siRAD51) was confirmed by an immunoblot analysis using anti-RAD51 antibodies. Hiroki Shima et al. J Cell Sci 2013;126:5284-5292 © 2013. Published by The Company of Biologists Ltd