IndraLab

"ATXN3L directly binds, deubiquitinates, and stabilizes KLF5."

"Finally, to test whether ATXN3L directly interacts with KLF5, we expressed and purified recombinant proteins, including KLF5-6xHis from E.coli and GST-ATXN3L from both HEK293FT cells and E.coli."

"To examine whether ATXN3L physically interacts with KLF5, we transfected Myc-ATXN3L and KLF5-3xFlag into HEK293FT cells and immunoprecipitated KLF5-3xFlag."

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"Finally, to test whether ATXN3L directly interacts with KLF5, we expressed and purified recombinant proteins, including KLF5-6×His from E.coli and GST-ATXN3L from both HEK293FT cells and E.coli ."

"ATXN3L interacts with KLF5."

"The ATXN3L protein interacted with the KLF5 protein and decreased the KLF5 polyubiquitination."

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"ATXN3L directly binds, deubiquitinates, and stabilizes KLF5."

"To examine whether ATXN3L physically interacts with KLF5, we transfected Myc-ATXN3L and KLF5-3×Flag into HEK293FT cells and immunoprecipitated KLF5-3×Flag."

"To further determine whether ATXN3L increases the KLF5 protein stability, we measured the KLF5 protein half-lives by the cycloheximide (CHX) chase assays [XREF_BIBR]."

"As expected, ATXN3L over-expression blocked the KLF5 protein degradation induced by WWP1 and FBW7."

"To test whether ATXN3L can antagonize E3 ligase mediated KLF5 degradation, we transfected WWP1, Myc-FBW7, KLF5 and ATXN3L into HEK293FT cells."

"To further confirm whether ATXN3L knockdown decreases KLF5 protein stability in human breast cancer cells, we knocked down ATXN3L in HCC1806 and SUM1315 (two basal type triple negative breast cancer cell lines), in which KLF5 is highly expressed."

"Collectively, these results suggest that ATXN3L is a specific DUB for KLF5 and that ATXN3L increases KLF5 protein stability through deubiquitination."

"ATXN3L deubiquitinates KLF5."

"Whether the deubiquitination of KLF5 protein by ATXN3L is regulated is unknown at present."

"We then sought to determine whether ATXN3L directly decreases the KLF5 ubiquitination."

"The ATXN3L protein interacted with the KLF5 protein and decreased the KLF5 polyubiquitination."

"Ataxin-3 like (ATXN3L), a member of the Josephin family of deubiquitinating enzymes, promotes breast cancer proliferation by deubiquitinating Kruppel-like factor 5 (KLF5). Ge F(1)(2), Chen W(3), Qin J(1), Zhou Z(1), Liu R(1), Liu L(4), Tan J(3), Zou T(3), Li H(2), Ren G(2), Chen C(1). Author information: (1)Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan, China. (2)Chongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. (3)Department of Breast Surgery, The 3rd Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China. (4)Laboratory for Conservation and Utilization of Bioresource, Yunnan University, Kunming, China. The Kr眉ppel-like factor 5 (KLF5) has been suggested to promote breast cell proliferation, survival and tumorigenesis."

"GST-ATXN3L, but not GST-ATXN3L (M4), dramatically decreased the KLF5 protein polyubiquitination."

"Although ATXN3L decreases the KLF5 protein ubiquitination, ATXN3L may have other substrate proteins."

"As shown in Figure XREF_FIG, ATXN3L silencing increased the endogenous KLF5 protein ubiquitination."

"As expected, knockdown of ATXN3L dramatically decreased the endogenous KLF5 protein levels in both cell lines."

"We identified ATXN3L as a candidate KLF5 DUB because knockdown of ATXN3L decreased KLF5 protein levels and inhibited breast cancer cell proliferation."

"As described above, knockdown of ATXN3L decreased the endogenous KLF5 protein levels in both HCC1806 and SUM1315 cell lines."

"Knockdown of ATXN3L decreased KLF5 protein levels and inhibited the proliferation of breast cancer cells [XREF_BIBR]."

"Nevertheless, ATXN3L increased the KLF5 protein stability and inhibited the expression of KLF5 downstream target genes, such as p21 and p27, and promote basal type breast cancer cell proliferation."

"ATXN3L was identified as a candidate KLF5 DUB because the siRNA pool, and 2 out of 3 individual siRNA, against ATXN3L dramatically decreased the KLF5 protein level in HeLa."

"GST-ATXN3L, but not GST-ATXN3L (M4), dramatically decreased the KLF5 protein polyubiquitination."

"As shown in Figure xref , ATXN3L silencing increased the endogenous KLF5 protein ubiquitination."

"Furthermore, knockdown of ATXN3L by two different siRNAs also upregulated p27 and p21 protein levels in these cell lines."

"Since ATXN3L stabilizes KLF5 and inhibits the expression of p27 and p21, it is plausible that ATXN3L also promotes breast cancer cell proliferation."

"Functionally, depletion of ATXN3L increased the p27 and p21 protein levels and suppressed breast cancer cell proliferation."