PTPIP51 is phosphorylated by Lyn and c-Src kinases lacking dephosphorylation by PTP1B in acute myeloid leukemia

Brobeil, Alexander; Bobrich, Manuel; Graf, Michaela; Kruchten, Anke; Blau, Wolfgang; Rummel, Mathias; Oeschger, Sabine; Steger, Klaus; Wimmer, Monika

doi:10.1016/j.leukres.2011.03.024

Cited by 16 publications

(32 citation statements)

References 31 publications

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“…[19][20][21][22][23][24][25][26][27] Among these, casp8, a cysteine protease known to trigger the extrinsic apoptotic pathway, is described as inhibited when the zymogen form, procasp8, is phosphorylated by SFKs at Tyr380. 21,22 To verify whether procasp8 was included in the set of Lyn-dependent tyrosine phosphorylated cytosolic substrates in B-CLL, the cytosol of leukemia cells from 12 patients (6 U-CLL and 6 M-CLL) underwent 2D-PAGE using a narrow linear range (pH 4-7) immobilized pH gradient in the first dimension to improve the resolution of the pTyr spots followed by Wb analysis with anti-pTyr antibody.…”

Section: Resultsmentioning

confidence: 99%

Lyn-mediated procaspase 8 dimerization blocks apoptotic signaling in B-cell chronic lymphocytic leukemia

Zonta

Pagano

Trentin

et al. 2014

Blood

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Section: Resultsmentioning

confidence: 99%

Lyn-mediated procaspase 8 dimerization blocks apoptotic signaling in B-cell chronic lymphocytic leukemia

Zonta

Pagano

Trentin

et al. 2014

Blood

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“…The absence of the 60 kDa phosphorylated PTPIP51 form 4 hours post synchronization probably hints to an involvement in mitotic processes. Two studies from our laboratory pointed to a regulation of the PTPIP51/Raf-1 interaction by tyrosine phosphorylation [8,9]. In cells of acute myeloid leukemia PTPIP51 is unable to interact with Raf-1 while phosphorylated at its tyrosine 176 residue [9].…”

Section: Discussionmentioning

confidence: 99%

“…Two studies from our laboratory pointed to a regulation of the PTPIP51/Raf-1 interaction by tyrosine phosphorylation [8,9]. In cells of acute myeloid leukemia PTPIP51 is unable to interact with Raf-1 while phosphorylated at its tyrosine 176 residue [9]. In general, this indicates a mechanism for conducting PTPIP51 to specific cellular compartments and specialized cellular functions.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, Brobeil and co-workers showed that Lyn, a member of the Src family kinases, also interacts with PTPIP51 in cells of acute myeloid leukemia [9]. Strikingly, during mitosis cdc2 phosphorylates c-Src at specific serine and threonine residues.…”

Section: Discussionmentioning

confidence: 99%

“…Highly tyrosine phosphorylated PTPIP51 also was observed in blasts of acute myeloid leukemia (AML). In addition, due to the lack of the phosphatase PTP1B, PTPIP51 cannot be dephophorylated in cells of AML [9]. These leukemic cells feature autonomous proliferation with a high mitotic index [10].…”

Section: Introductionmentioning

confidence: 99%

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Interaction of PTPIP51 with Tubulin, CGI-99 and Nuf2 During Cell Cycle Progression

et al. 2012

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Protein tyrosine phosphatase interacting protein 51 (PTPIP51), also known as regulator of microtubule dynamics protein 3, was identified as an in vitro and in vivo interaction partner of CGI-99 and Nuf-2. PTPIP51 mRNA is expressed in all stages of the cell cycle; it is highly expressed six hours post-nocodazole treatment and minimally expressed one hour post-nocodazole treatment. Recent investigations located PTPIP51 protein at the equatorial plate. This study reports the localization of the PTPIP51/CGI-99 and the PTPIP51/Nuf-2 complex at the equatorial region during mitosis. Moreover, Duolink proximity ligation assays revealed an association of PTPIP51 with the microtubular cytoskeleton and the spindle apparatus. High amounts of phosphorylated PTPIP51 associated with the spindle poles was seen by confocal microscopy. In parallel a strong interaction of PTPIP51 with the epidermal growth factor receptor phosphorylating PTPIP51 at the tyrosine 176 residue was seen. In the M/G1 transition a high level of interaction between PTPIP51 and PTP1B was registered, thus restoring the interaction of PTPIP51 and Raf-1, depleted in mitotic cells. Summarizing these new facts, we conclude that PTPIP51 is necessary for normal mitotic processes, impacting on chromosomal division and control of the MAPK pathway activity.

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Identification of distinctive long noncoding RNA competitive interactions and a six‐methylated‐gene prognostic signature in acute myeloid leukemia with −5/del(5q) or −7/del(7q)

Yin

Huang

et al. 2019

J of Cellular Biochemistry

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Background Acute myeloid leukemia (AML) with −5/del(5q) or −7/del(7q) has special clinical and biological characteristics, but its molecular mechanisms and risk stratification remain unknown. Methods The RNA sequencing and DNA methylation of 23 patients with −5/del(5q) or −7/del(7q) and 128 patients with other subtypes of acute myeloid leukemia were obtained from The Cancer Genome Atlas (TCGA). The regulatory mechanisms of competitive endogenous RNA (ceRNA) network and DNA methylation on gene expression were explored. To find robust and specific risk stratification for this AML subtype, a prognostic model was established and evaluated through four independent data sets. Results We identified 966 differentially expressed long noncoding RNA, 2274 differentially expressed genes, and 47 differentially expressed microRNAs, and constructed a ceRNA network. After the integrated analysis of differentially methylated and expressed genes, 19 genes showed the opposite trend between the methylation variation and gene expression. An six‐methylated‐gene prognostic signature which highly correlated with overall survival was established, and the performance was validated by leave‐one‐out cross validation method and permutation test. Furthermore, the excellent prognostic value of this model was supported by an independent cohort, while specificity of this model was validated by three independent data sets, suggesting it as a predictive classifier with high efficiency for distinguishing those with −5/del(5q) or −7/del(7q) from other AML subtypes. Conclusions The ceRNA network may provide new ideas for the diagnosis and treatment for patients with −5/del(5q) or −7/del(7q).The six‐methylated‐gene prognostic signature was a robust, specific, and clinically practical risk stratification for the outcome of patients with AML having −5/del(5q) or −7/del(7q).

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PTPIP51 is phosphorylated by Lyn and c-Src kinases lacking dephosphorylation by PTP1B in acute myeloid leukemia

Cited by 16 publications

References 31 publications

Lyn-mediated procaspase 8 dimerization blocks apoptotic signaling in B-cell chronic lymphocytic leukemia

Lyn-mediated procaspase 8 dimerization blocks apoptotic signaling in B-cell chronic lymphocytic leukemia

Interaction of PTPIP51 with Tubulin, CGI-99 and Nuf2 During Cell Cycle Progression

Identification of distinctive long noncoding RNA competitive interactions and a six‐methylated‐gene prognostic signature in acute myeloid leukemia with −5/del(5q) or −7/del(7q)

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