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PDZ binding kinase

pBK, TOPK, PDZ-binding kinase, T-LAK cell-originated protein kinase
This genes encodes a serine/threonine kinase related to the dual specific mitogen-activated protein kinase kinase (MAPKK) family. Evidence suggests that mitotic phosphorylation is required for its catalytic activity. This mitotic kinase may be involved in the activation of lymphoid cells and support testicular functions, with a suggested role in the process of spermatogenesis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, Lak, HAD, ACID, V1a
Papers using pBK antibodies
Mutant ubiquitin found in neurodegenerative disorders is a ubiquitin fusion degradation substrate that blocks proteasomal degradation
Dantuma Nico P. et al., In The Journal of Cell Biology, 1994
... open reading frames were expressed from a CMV promoter in the mammalian expression vectors pcDNA3 (Invitrogen), pBK-CMV (Stratagene), EGFP-N1, or pCMS-EGFP (CLONTECH Laboratories, Inc.) ...
Papers on pBK
TOPK promotes lung cancer resistance to EGFR tyrosine kinase inhibitors by phosphorylating and activating c-Jun.
Li et al., Xi'an, China. In Oncotarget, Feb 2016
The present study shows that T-lymphokine-activated killer cell-originated protein kinase (TOPK) is upregulated in NSCLC and excessively activated in TKI-refractory cells.
p21 induction plays a dual role in anti-cancer activity of ursolic acid.
Hu et al., Beijing, China. In Exp Biol Med (maywood), Dec 2015
Moreover, we found that ursolic acid was able to inhibit murine double minute-2 protein (MDM2) and T-LAK cell-originated protein kinase (TOPK), the two negative regulator of p53, which in turn contributed to ursolic acid-induced p53 activation.
Overexpression of PDZ-binding kinase confers malignant phenotype in prostate cancer via the regulation of E2F1.
Zhong et al., Guangzhou, China. In Int J Biol Macromol, Nov 2015
To address this problem, we here identified PDZ-binding kinase (PBK) as a direct target for E2F1 through bioinformatics binding site prediction, combined with chromatin immunoprecipitation-PCR (ChIP-PCR), quantitative (Q)-PCR and Western blot analysis.
T-LAK cell-originated protein kinase presents a novel therapeutic target in FLT3-ITD mutated acute myeloid leukemia.
Nakamura et al., Chicago, United States. In Oncotarget, Nov 2015
Here we show that T-LAK cell-originated protein kinase (TOPK), a mitotic kinase highly expressed in and correlated with more aggressive phenotype in several types of cancer, is expressed in AML but not in normal CD34+ cells and that TOPK knockdown decreased cell viability and induced apoptosis.
EBP50 inhibits pancreatic cancer cell growth and invasion by targeting the β-catenin/E-cadherin pathway.
Peng et al., Wuhan, China. In Exp Ther Med, Oct 2015
Furthermore, pBK-CMV-HA-EBP50 and the pBK-CMV-HA vectors were transfected into pancreatic cancer cells and the effect of EBP50 upregulation on the proliferation and invasion of the cells was investigated.
PBK/TOPK mediates promyelocyte proliferation via Nrf2-regulated cell cycle progression and apoptosis.
Zhang et al., Xi'an, China. In Oncol Rep, Oct 2015
PBK/TOPK is a protein kinase derived from PDZ-binding kinase (PBK)/T-lymphokine-activated killer (T-LAK) cell-originated protein kinase (TOPK).
Combined expressional analysis, bioinformatics and targeted proteomics identify new potential therapeutic targets in glioblastoma stem cells.
Langmoen et al., Oslo, Norway. In Oncotarget, Oct 2015
Bioinformatic filtering identified 20 genes (PBK/TOPK, CENPA, KIF15, DEPDC1, CDC6, DLG7/DLGAP5/HURP, KIF18A, EZH2, HMMR/RHAMM/CD168, NOL4, MPP6, MDM1, RAPGEF4, RHBDD1, FNDC3B, FILIP1L, MCC, ATXN7L4/ATXN7L1, P2RY5/LPAR6 and FAM118A) that were consistently expressed in GSC cultures and consistently not expressed in NSC cultures.
Effect of the efflux pump QepA2 combined with chromosomally mediated mechanisms on quinolone resistance and bacterial fitness in Escherichia coli.
Rodríguez-Martínez et al., Madrid, Spain. In J Antimicrob Chemother, Sep 2015
METHODS: E. coli ATCC 25922 and derived isogenic strains harbouring different chromosomally mediated fluoroquinolone resistance determinants were electroporated with pBK-CMV vector encoding QepA2.
PBK/TOPK enhances aggressive phenotype in prostate cancer via β-catenin-TCF/LEF-mediated matrix metalloproteinases production and invasion.
Banerjee et al., Washington, D.C., United States. In Oncotarget, Jul 2015
The aim of this study was to evaluate the role of PDZ Domain-binding kinase (PBK) in prostate cancer and to determine if PBK expression enhances aggressiveness in prostate cancer.
CXCL8, overexpressed in colorectal cancer, enhances the resistance of colorectal cancer cells to anoikis.
Li et al., Kunming, China. In Cancer Lett, Jun 2015
Here, we found that a high abundance of CXCL8 or TOPK strongly correlated with poor overall and disease-free survival of 186 patients with CRC.
TOPK is highly expressed in circulating tumor cells, enabling metastasis of prostate cancer.
Shao et al., Xi'an, China. In Oncotarget, Jun 2015
T-LAK cell-originated protein kinase (TOPK) is highly expressed in cancer cells.
Identification of the oncogenic kinase TOPK/PBK as a master mitotic regulator of C2H2 zinc finger proteins.
Hurt et al., Tallahassee, United States. In Oncotarget, Mar 2015
TOPK/PBK is an oncogenic kinase upregulated in most human cancers and its high expression correlates with poor prognosis.
Targeting PBK/TOPK decreases growth and survival of glioma initiating cells in vitro and attenuates tumor growth in vivo.
Stangeland et al., Oslo, Norway. In Mol Cancer, 2014
Here, we investigate a protein kinase, PBK/TOPK as a candidate for regulating growth, survival and in vivo tumorigenicity of GICs.
PBK/TOPK mediates geranylgeranylation signaling for breast cancer cell proliferation.
Lin et al., Zhenjiang, China. In Cancer Cell Int, 2014
PDZ binding-kinase (PBK) (also named T-lymphokine-activated killer cell-originated protein kinase (TOPK)), a serine/threonine kinase, is tightly controlled in normal tissues but elevated in many tumors, and functions in tumorigenesis and metastasis.
Expression of PBK/TOPK in cervical cancer and cervical intraepithelial neoplasia.
Shen et al., Guangzhou, China. In Int J Clin Exp Pathol, 2013
UNLABELLED: objectives: To evaluate the expression of PBK/TOPK (PDZ-binding kinase/T-LAK cell-originated protein kinase) and its clinical significance in cervical cancer and cervical intraepithelial neoplasia.
Overexpression of T-LAK cell-originated protein kinase predicts poor prognosis in patients with stage I lung adenocarcinoma.
Lai et al., Taipei, Taiwan. In Cancer Sci, 2012
Our results indicate that overexpression of TOPK could predetermine the metastatic capability of tumors and could serve as a significant prognostic predictor of shortened overall survival and time to recurrence.
T-LAK cell-originated protein kinase (TOPK) phosphorylation of MKP1 protein prevents solar ultraviolet light-induced inflammation through inhibition of the p38 protein signaling pathway.
Dong et al., Austin, United States. In J Biol Chem, 2011
T-LAK cell-originated protein kinase (TOPK) phosphorylation of MKP1 protein prevents solar ultraviolet light-induced inflammation through inhibition of the p38 protein signaling pathway.
PBK/TOPK interacts with the DBD domain of tumor suppressor p53 and modulates expression of transcriptional targets including p21.
Rapoport et al., Baltimore, United States. In Oncogene, 2010
increased levels of PBK/TOPK may contribute to tumor cell development and progression through suppression of p53 function and consequent reductions in the cell-cycle regulatory proteins such as p21.
Critical roles of LGN/GPSM2 phosphorylation by PBK/TOPK in cell division of breast cancer cells.
Nakamura et al., Tokyo, Japan. In Genes Chromosomes Cancer, 2010
Upregulation of TOPK is associated with breast cancer.
T-LAK cell-originated protein kinase (TOPK) phosphorylation of Prx1 at Ser-32 prevents UVB-induced apoptosis in RPMI7951 melanoma cells through the regulation of Prx1 peroxidase activity.
Dong et al., Austin, United States. In J Biol Chem, 2010
Phosphorylation of Prx1 (Ser-32) by TOPK prevents UVB-induced apoptosis in RPMI7951 melanoma cells through regulation of Prx1 peroxidase activity and blockade of intracellular H(2)O(2) accumulation.
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