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An, Yujin,Oh, Jiyeon,Chen, Shanshan,Lee, Byongkyu,Lee, Sang Myeon,Han, Daehee,Yang, Changduk The Royal Society of Chemistry 2018 Polymer chemistry Vol.9 No.5
<P>A new family of naphthalenediimide (NDI)-bithiophene-based random terpolymers (PNDI-Fu10, PNDI-Th10, and PNDI-Se10) was prepared by incorporating a small amount (10 mol%) of different chalcogenophene units, namely furan (Fu), thiophene (Th), and selenophene (Se), into a poly((<I>N</I>,<I>N</I>’-bis(2-octyldodecyl)-naphthalene-1,4,5,8-bis(dicarboximide)-2,6-diyl)-<I>alt</I>-5,5′-(2,2′-bithiophene)) (P(NDI2OD-T2)) backbone. The terpolymers all exhibited negligible optical property and frontier energy level differences. Interestingly, the blend film morphology and photovoltaic performance of all-polymer solar cells (all-PSCs), comprising a random terpolymer series as an acceptor and poly(6-fluoro-2,3-bis-(3-octyloxyphenyl)quinoxaline-5,8-dyl-<I>alt</I>-thiophene-2,5-diyl) (FTQ) as a donor, were strongly dependent on the type of chalcogenophene. Consequently, the all-PSCs revealed a clear variation in short-circuit current density (<I>J</I>SC) and fill factor (FF) while retaining identical open-circuit voltages (<I>V</I>OC). The greatest power-conversion efficiency of 5.88% with a high <I>J</I>SC of 10.77 mA cm<SUP>−2</SUP> was observed for PNDI-Th10:FTQ because of a synergistic contribution from a more preferential π-face-on orientation and suppression of bimolecular/geminate recombination. This was confirmed by a detailed investigation on the morphology and charge dynamic structural properties. In addition to understanding their effects on photovoltaic characteristics, this study demonstrates that introducing a small amount of the chalcogenophenes into a well-performing polymer is a simple and effective method to improve <I>J</I>SC values while maintaining <I>V</I>OCs of the parent polymers.</P>
An-Chen Lee,Tzu-Wei Kuo,Chung-Ting Ma 한국정밀공학회 2012 International Journal of Precision Engineering and Vol. No.
In this paper, we proposed a control strategy: Combined Product and Tool Disturbance Estimator (CPTDE) which combines threaded double EWMA with the drift compensation scheme, to adaptively estimate the disturbance for a mixproduct situation in semiconductor processes. This approach considers the disturbances are related to the combination of the specific product and the tool, and further separates the error into an intercept term and a drift term, where the former is related to the variation of products, whereas the latter is related to the interaction between the tools and the products. The proposed method continuously updates the intercept and drift terms to obtain the recipe for the next run. The simulation case studies, i.e., the fixed schedule process, the random schedule process, and the periodical schedule process, are conducted and the results show that CPTDE control scheme has best control performance when compared with three recently published control schemes. The method is also applied to the estimation of removal rate in mix-product CMP process. The results show that the proposed method has improvements over product-based EWMA control, CF-EWMA control and threaded PCC control by 9.52%, 2523.43% and 11.71% on average, respectively, for estimating removal rate of historical data in mix-product CMP process.
FBXW7-mediated ERK3 degradation regulates the proliferation of lung cancer cells
An Hyun-Jung,Lee Cheol-Jung,Lee Ga-Eun,Choi Youngwon,Jeung Dohyun,Chen Weidong,Lee Hye Suk,강한창,이주영,Kim Dae Joon,Choi Jin-Sung,Cho Eun Suh,Choi Jong-Soon,조용연 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Extracellular signal-regulated kinase 3 (ERK3) is an atypical member of the mitogen-activated protein kinase (MAPK) family, members of which play essential roles in diverse cellular processes during carcinogenesis, including cell proliferation, differentiation, migration, and invasion. Unlike other MAPKs, ERK3 is an unstable protein with a short half-life. Although deubiquitination of ERK3 has been suggested to regulate the activity, its ubiquitination has not been described in the literature. Here, we report that FBXW7 (F-box and WD repeat domain-containing 7) acts as a ubiquitination E3 ligase for ERK3. Mammalian two-hybrid assay and immunoprecipitation results demonstrated that ERK3 is a novel binding partner of FBXW7. Furthermore, complex formation between ERK3 and the S-phase kinase-associated protein 1 (SKP1)-cullin 1-F-box protein (SCF) E3 ligase resulted in the destabilization of ERK3 via a ubiquitination-mediated proteasomal degradation pathway, and FBXW7 depletion restored ERK3 protein levels by inhibiting this ubiquitination. The interaction between ERK3 and FBXW7 was driven by binding between the C34D of ERK3, especially at Thr417 and Thr421, and the WD40 domain of FBXW7. A double mutant of ERK3 (Thr417 and Thr421 to alanine) abrogated FBXW7-mediated ubiquitination. Importantly, ERK3 knockdown inhibited the proliferation of lung cancer cells by regulating the G1/S-phase transition of the cell cycle. These results show that FBXW7-mediated ERK3 destabilization suppresses lung cancer cell proliferation in vitro.
Dysregulated CREB3 cleavage at the nuclear membrane induces karyoptosis-mediated cell death
Lee Ga-Eun,Bang Geul,Byun Jiin,Lee Cheol-Jung,Chen Weidong,Jeung Dohyun,An Hyun-Jung,Kang Han Chang,Lee Joo Young,Lee Hye Suk,Hong Young-Soo,Kim Dae Joon,Keniry Megan,Kim Jin Young,Choi Jin-Sung,Fanto 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
Cancer cells often exhibit resistance to apoptotic cell death, but they may be vulnerable to other types of cell death. Elucidating additional mechanisms that govern cancer cell death is crucial for developing new therapies. Our research identified cyclic AMP-responsive element-binding protein 3 (CREB3) as a crucial regulator and initiator of a unique cell death mechanism known as karyoptosis. This process is characterized by nuclear shrinkage, deformation, and the loss of nuclear components following nuclear membrane rupture. We found that the N-terminal domain (aa 1-230) of full-length CREB3 (CREB3-FL), which is anchored to the nuclear inner membrane (INM), interacts with lamins and chromatin DNA. This interaction maintains a balance between the outward force exerted by tightly packed DNA and the inward constraining force, thereby preserving INM integrity. Under endoplasmic reticulum (ER) stress, aberrant cleavage of CREB3-FL at the INM leads to abnormal accumulation of the cleaved form of CREB3 (CREB3-CF). This accumulation disrupts the attachment of CREB3-FL to the INM, resulting in sudden rupture of the nuclear membrane and the onset of karyoptosis. Proteomic studies revealed that CREB3-CF overexpression induces a DNA damage response akin to that caused by UVB irradiation, which is associated with cellular senescence in cancer cells. These findings demonstrated that the dysregulation of CREB3-FL cleavage is a key factor in karyoptotic cell death. Consequently, these findings suggest new therapeutic strategies in cancer treatment that exploit the process of karyoptosis.
Jih-Jong Lee,Han-You Lin,Chun-An Chen,Chen-Si Lin,Lih-Chiann Wang 대한수의학회 2019 Journal of Veterinary Science Vol.20 No.1
Canine MDR1 gene mutations produce translated P-glycoprotein, an active drug efflux transporter, resulting in dysfunction or over-expression. The 4-base deletion at exon 4 of MDR1 at nucleotide position 230 (nt230[del4]) in exon 4 makes P-glycoprotein lose function, leading to drug accumulation and toxicity. The G allele of the c.-6-180T>G variation in intron 1 of MDR1 (single nucleotide polymorphism [SNP] 180) causes P-glycoprotein over-expression, making epileptic dogs resistant to phenobarbital treatment. Both of these mutations are reported to be common in collies. This study develops a more efficient method to detect these two mutations simultaneously, and clarifies the genotype association with the side effects of chemotherapy. Genotype distribution in Taiwan was also investigated. An oligonucleotide microarray was successfully developed for the detection of both genotypes and was applied to clinical samples. No 4-base deletion mutant allele was detected in dogs in Taiwan. However, the G allele variation of SNP 180 was spread across all dog breeds, not only in collies. The chemotherapy adverse effect percentages of the SNP 180 T/T, T/G, and G/G genotypes were 16.7%, 6.3%, and 0%, respectively. This study describes an efficient way for MDR1 gene mutation detection, clarifying genotype distribution, and the association with chemotherapy.