A systematic study of nuclear interactome of C-terminal domain small phosphatase-like 2 using inducible expression system and shotgun proteomics

Kang, NaNa; Koo, JaeHyung; Wang, Sen; Hur, Sun; Bahk, Young Yil

doi:10.5483/bmbrep.2016.49.6.240

Cited by 7 publications

(5 citation statements)

References 25 publications

(35 reference statements)

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“…In accord with prior studies (Kemmer et al, 2006;Zhao et al, 2014;Kang et al, 2016), we found that SCP4 was localized to the nucleus of AML cells (Figure 4A). However, our efforts at performing SCP4 chromatin immunoprecipitation sequencing (ChIP-seq) in MOLM-13 cells failed to identify evidence of sequence-specific DNA occupancy (data not shown).…”

Section: Stk35 and Pdik1l Bind Selectively To The Catalytically Active Form Of Scp4supporting

confidence: 92%

SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia

et al. 2022

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Section: Stk35 and Pdik1l Bind Selectively To The Catalytically Active Form Of Scp4supporting

confidence: 92%

SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia

et al. 2022

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“…In accord with prior studies (Kemmer et al, 2006;Zhao et al, 2014;Kang et al, 2016), we found that SCP4 was localized to the nucleus of AML cells (Figure 4A). However, our efforts at performing SCP4 ChIP-seq in MOLM-13 cells failed to identify evidence of sequence-specific DNA occupancy (data not shown).…”

Section: Stk35 and Pdik1l Bind Selectively To The Catalytically Active Form Of Scp4supporting

confidence: 92%

The SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia

Polyanskaya

et al. 2021

Preprint

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Acute myeloid leukemia (AML) cells rely on phospho-signaling pathways to gain unlimited proliferation potential. Here, we used domain-focused CRISPR screening to identify the nuclear phosphatase SCP4 as a dependency in AML, yet this enzyme is dispensable in normal hematopoietic progenitor cells. Using CRISPR exon scanning and gene complementation assays, we show that the catalytic function of SCP4 is essential in AML. Through mass spectrometry analysis of affinity-purified complexes, we identify the kinase paralogs STK35 and PDIK1L as binding partners and substrates of the SCP4 phosphatase domain. We show that STK35 and PDIK1L function catalytically and redundantly in the same pathway as SCP4 to maintain AML proliferation and to support amino acid biosynthesis and transport. We provide evidence that SCP4 regulates STK35/PDIK1L through two distinct mechanisms: catalytic removal of inhibitory phosphorylation and by promoting kinase stability. Our findings reveal a phosphatase-kinase signaling complex that supports the pathogenesis of AML.

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“…Coimmunoprecipitation analysis was performed as described previously [ 41 ]. In brief, 500 μg of cellular proteins were incubated with immunoprecipitating antibodies in extraction buffer for 6 h at 4 °C.…”

Section: Methodsmentioning

confidence: 99%

Induction of p53-Independent Apoptosis and G1 Cell Cycle Arrest by Fucoidan in HCT116 Human Colorectal Carcinoma Cells

Park

Jeong

et al. 2017

Marine Drugs

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Abstract:It is well known that fucoidan, a natural sulfated polysaccharide present in various brown algae, mediates anticancer effects through the induction of cell cycle arrest and apoptosis. Nevertheless, the role of tumor suppressor p53 in the mechanism action of fucoidan remains unclear. Here, we investigated the anticancer effect of fucoidan on two p53 isogenic HCT116 (p53+/+ and p53−/−) cell lines. Our results showed that inhibition of cell viability, induction of apoptosis and DNA damage by treatment with fucoidan were similar in two cell lines. Flow cytometric analysis revealed that fucoidan resulted in G1 arrest in the cell cycle progression, which correlated with the inhibition of phosphorylation of retinoblastoma protein (pRB) and concomitant association of pRB with the transcription factor E2Fs. Furthermore, treatment with fucoidan obviously upregulated the expression of cyclin-dependent kinase (CDK) inhibitors, such as p21WAF1/CIP1 and p27KIP1, which was paralleled by an enhanced binding with CDK2 and CDK4. These events also commonly occurred in both cell lines, suggesting that fucoidan triggered G1 arrest and apoptosis in HCT116 cells by a p53-independent mechanism. Thus, given that most tumors exhibit functional p53 inactivation, fucoidan could be a possible therapeutic option for cancer treatment regardless of the p53 status.

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A systematic study of nuclear interactome of C-terminal domain small phosphatase-like 2 using inducible expression system and shotgun proteomics

Cited by 7 publications

References 25 publications

SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia

SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia

The SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia

Induction of p53-Independent Apoptosis and G1 Cell Cycle Arrest by Fucoidan in HCT116 Human Colorectal Carcinoma Cells

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