Stable interactors of Plk1 include phosphorylation-dependent interactions. Stable interactors of Plk1 include phosphorylation-dependent interactions. (A)

Slides:

Advertisements

Similar presentations

Scott Rusin Kettenbach Lab NERIC 2017 August 18th 2017

Advertisements

Volume 11, Issue 4, Pages (April 2003)

Volume 45, Issue 5, Pages (March 2012)

by Katriina J. Peltola, Kirsi Paukku, Teija L. T

Pirh2 promotes p73 ubiquitination in vivo.

The evolutionary conserved cassette ABBA1-KEN2-ABBA2 in BUBR1 is essential for SAC signalling. The evolutionary conserved cassette ABBA1-KEN2-ABBA2 in.

90K Glycoprotein Promotes Degradation of Mutant β-Catenin Lacking the ISGylation or Phosphorylation Sites in the N-terminus So-Yeon Park, Somy Yoon,

Shitao Li, Lingyan Wang, Michael A. Berman, Ye Zhang, Martin E. Dorf

Volume 14, Issue 5, Pages (May 2008)

Volume 31, Issue 3, Pages (August 2008)

Volume 22, Issue 5, Pages (May 2012)

Binding of Pentamer to cells.

Volume 19, Issue 5, Pages (May 2012)

Volume 36, Issue 4, Pages (November 2009)

NuMA directly interacts with Plk1 and gets phosphorylated at its C-terminus. NuMA directly interacts with Plk1 and gets phosphorylated at its C-terminus.

Bimodal Binding of STIL to Plk4 Controls Proper Centriole Copy Number

Stefanie S. Schalm, Diane C. Fingar, David M. Sabatini, John Blenis

Frequency distribution of the GRAVY of the theoretical proteins (open bars) and of 110 genes encoding proteins identified on a 2-D electrophoresis gel,

PKA phosphorylates Thr63 and Ser692 to increase HIF-1α stability.

PKA interacts with HIF-1α.

MAGE-RING Protein Complexes Comprise a Family of E3 Ubiquitin Ligases

Plk1 negatively regulates NuMA cortical localization by phosphorylating at its C-terminus. Plk1 negatively regulates NuMA cortical localization by phosphorylating.

Volume 56, Issue 5, Pages (December 2014)

Plk1 inhibition or depletion causes robust cortical NuMA localization in mitosis. Plk1 inhibition or depletion causes robust cortical NuMA localization.

Substrate-Specific Activation of the Mitotic Kinase Bub1 through Intramolecular Autophosphorylation and Kinetochore Targeting Zhonghui Lin, Luying Jia,

The Tumor Suppressor MIG6 Controls Mitotic Progression and the G2/M DNA Damage Checkpoint by Stabilizing the WEE1 Kinase Mari Sasaki, Takeshi Terabayashi,

Structural analysis of the hypoxanthine phosphoribosyltransferase (HPRT) Ser162Thr mutation. Structural analysis of the hypoxanthine phosphoribosyltransferase.

Volume 24, Issue 4, Pages e5 (April 2017)

p38 MAPK activation is required for phosphorylation of Akt at Ser473.

Sara K. Donnelly, Ina Weisswange, Markus Zettl, Michael Way

Volume 36, Issue 6, Pages (December 2009)

Volume 14, Issue 3, Pages (May 2004)

Overlap between changes in de novo protein synthesis after p53- or miR-34a-induction. Overlap between changes in de novo protein synthesis after p53- or.

ONC201 activates the ATF4 pathway through the eIF2α kinases HRI and PKR. ONC201 activates the ATF4 pathway through the eIF2α kinases HRI and PKR. (A) Western.

Regulation of PP6 phosphatase activity by Plk1 in vitro.

Plk1 inhibition affects the NuMA turnover at the spindle pole.

Volume 43, Issue 3, Pages (August 2011)

Fig. 2 Cross-modal recognition between echolocation and vision.

14-3-3γ phosphorylated at S59 by Lats2 in response to UV damage.

Dissociation of HP1α from H3K9me3 is critical to potentiation of steady-state ATM activity. Dissociation of HP1α from H3K9me3 is critical to potentiation.

Relative expression levels of three PTPN22 transcripts.

The wild-type BRCA1-BARD1 EM structure resembles a clamp-like motif

Global analysis of RV[S/T]F motif phosphorylation during mitosis.

PP1 preferentially binds nonphosphorylated RV[S/T]F motifs in vitro.

Smad oligomerisation. Smad oligomerisation. Pictorial representation of the plasma membrane receptor kinases that phosphorylate the C-termini of R-Smads.

MYC degradation screen identifies a compound that stabilizes MYC protein. MYC degradation screen identifies a compound that stabilizes MYC protein. (A)

Effect of ERα Ub-binding ability on E2-induced receptor transcriptional activity. Effect of ERα Ub-binding ability on E2-induced receptor transcriptional.

PKM2 is tyrosine phosphorylated and inhibited by FGFR1 in cancer cells with oncogenic or overexpressed FGFR1. PKM2 is tyrosine phosphorylated and inhibited.

Phosphorylation of CBP by IKKα Promotes Cell Growth by Switching the Binding Preference of CBP from p53 to NF-κB Wei-Chien Huang, Tsai-Kai Ju, Mien-Chie.

Fig. 1 SAMTOR interacts with GATOR1 and KICSTOR.

Fig. 3 Proteomic analysis and Western blot analysis of protein cargos of various EVs. Proteomic analysis and Western blot analysis of protein cargos of.

Fig. 2 Nucleation is maintained but spreading is inhibited by roscovitine treatment. Nucleation is maintained but spreading is inhibited by roscovitine.

Mapping the Pirh2 and p73 interaction sites.

Association of CNK1 with Rho Guanine Nucleotide Exchange Factors Controls Signaling Specificity Downstream of Rho Aron B. Jaffe, Alan Hall, Anja Schmidt

Volume 16, Issue 14, Pages (July 2006)

CDCP1 links Ras and SFK signaling and regulates anoikis resistance, cell migration, and invasion in NSCLC cells. CDCP1 links Ras and SFK signaling and.

TET2 interacts with KLF1 transcription factor.

PTB-independent ShcA pools require a functional SH2 domain, but not the tyrosine phosphorylation sites to promote mammary tumorigenesis. PTB-independent.

HPV–human protein network map.

Fig. 1 Mmp-2 activity is increased in brains after HFD intake.

UNC drives MYC protein loss.

BCR/ABL expression, tyrosine phosphorylation, and signaling in dasatinib- and imatinib-resistant cell lines and the ubiquitin inhibitor lactacystin modifies.

Fig. 6 The C9ORF72/SMCR8 complex regulates ULK1.

Fig. 1 Schematic depiction of a paradigm for rapid and guided discovery of materials through iterative combination of ML with HiTp experimentation. Schematic.

Stable Cx43 expression in infected Cx43−/− cells and phosphorylation of Cx43. Stable Cx43 expression in infected Cx43−/− cells and phosphorylation of Cx43.

Fig. 2 Spatial distribution of five city groups.

Expression of PKM2 Y105F mutant in H1299 cells leads to decreased proliferation under hypoxic conditions, increased oxidative phosphorylation and reduced.

Fig. 3 Gene expression analysis in 48-plex drug treatment experiments.

An NH2-terminal domain of PALB2, distinct from the BRCA2-interacting domain of PALB2, mediates interaction with BRCA1 and assembly of PALB2 nuclear foci.

Fig. 5 Enhancers and super-enhancers identified in various brain cell populations. Enhancers and super-enhancers identified in various brain cell populations.

Presentation transcript:

Stable interactors of Plk1 include phosphorylation-dependent interactions. Stable interactors of Plk1 include phosphorylation-dependent interactions. (A) Diagram depicting the distribution of kinase inhibitor–sensitive (yellow) and kinase inhibitor–insensitive (blue) Plk1 interactors and, below, their relative enrichment in candidate PBD motifs [Ser-Ser-Pro (SSP)/Ser-Thr-Pro (STP); dark gray] or not (light gray). (B) Experimental design to identify kinase activity–dependent Plk1 interactors using wild-type and Pincer mutant Plk1. HeLa cells expressing with Myc- or Flag-tagged wild-type or Pincer mutant Plk1 were arrested in mitosis and treated with MG132. Plk1 and its interacting proteins were immunoprecipitated, resolved by gel electrophoresis, and analyzed by LC-MS/MS. (C) Diagram depicting the distribution of kinase inhibitor–sensitive (yellow) and kinase inhibitor–insensitive (blue) Plk1 interactors and their ability to bind (white) or not bind (black) to Pincer mutant Plk1. Arminja N. Kettenbach et al., Sci. Signal. 2018;11:eaaq1441 ©2018 by American Association for the Advancement of Science