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Mizuno, Rurie*; Niikura, Megumi*; Saito, Takeshi*; Matsuzaki, Teiichiro*; Sakurai, Hiroyoshi*; Amato, A.*; Asari, Shunsuke*; Biswas, S.*; Chiu, I.-H. ; Gianluca, J.*; et al.
Nuclear Instruments and Methods in Physics Research A, 1060, p.169029_1 - 169029_14, 2024/03
Rathore, E.*; Juneja, R.*; Sarkar, D.*; Roychowdhury, S.*; Kofu, Maiko; Nakajima, Kenji; Singh, A. K.*; Biswas, K.*
Materials Today Energy (Internet), 24, p.100953_1 - 100953_9, 2022/03
Times Cited Count:12 Percentile:87.17(Chemistry, Physical)Schmitt, C.*; Lemasson, A.*; Schmidt, K.-H.*; Jhingan, A.*; Biswas, S.*; Kim, Y. H.*; Ramos, D.*; Andreyev, A. N.; Curien, D.*; Ciemala, M.*; et al.
Physical Review Letters, 126(13), p.132502_1 - 132502_6, 2021/04
Times Cited Count:13 Percentile:83.62(Physics, Multidisciplinary)Laskar, Md. S. R.*; Saha, S.*; Palit, R.*; Mishra, S. N.*; Shimizu, Noritaka*; Utsuno, Yutaka; Ideguchi, Eiji*; Naik, Z.*; Babra, F. S.*; Biswas, S.*; et al.
Physical Review C, 99(1), p.014308_1 - 014308_6, 2019/01
Times Cited Count:6 Percentile:60.34(Physics, Nuclear)no abstracts in English
Jentschel, M.*; Blanc, A.*; de France, G.*; Kster, U.*; Leoni, S.*; Mutti, P.*; Simpson, G.*; Soldner, T.*; Ur, C.*; Urban, W.*; et al.
Journal of Instrumentation (Internet), 12(11), p.P11003_1 - P11003_33, 2017/11
Times Cited Count:34 Percentile:84.59(Instruments & Instrumentation)Biswas, K. K.*; Hase, Yoshihiro; Ono, Yutaka
JAEA-Review 2014-050, JAEA Takasaki Annual Report 2013, P. 113, 2015/03
Biswas, K. K.*; Hase, Yoshihiro; Narumi, Issey*; Ono, Yutaka
JAEA-Review 2013-059, JAEA Takasaki Annual Report 2012, P. 107, 2014/03
Biswas, K.; Mori, Takeshi*; Kogawara, Satoshi*; Narumi, Issei; Ono, Yutaka
JAEA-Review 2012-046, JAEA Takasaki Annual Report 2011, P. 100, 2013/01
Biswas, K.; Mori, Takeshi*; Kogawara, Satoshi*; Hase, Yoshihiro; Narumi, Issei; Ono, Yutaka
American Journal of Plant Sciences, 3(9), p.1181 - 1186, 2012/09
Nakasone, Akari*; Fujiwara, Masayuki*; Fukao, Yoichiro*; Biswas, K.; Rahman, A.*; Yamada, Maki*; Narumi, Issei; Uchimiya, Hirofumi*; Ono, Yutaka
Plant Physiology, 160(1), p.93 - 105, 2012/09
Times Cited Count:12 Percentile:38.8(Plant Sciences)Biswas, K.; Ono, Yutaka
Biological Sciences in Space, 25(2-4), p.45 - 55, 2011/12
Biswas, K. K.*; Oura, Chiharu*; Higuchi, Kanako*; Miyazaki, Yuji*; Nguyen, V. V.*; Rahman, A.*; Uchimiya, Hirofumi*; Kiyosue, Tomohiro*; Koshiba, Tomokazu*; Tanaka, Atsushi; et al.
Plant Physiology, 145(3), p.773 - 785, 2007/11
Times Cited Count:37 Percentile:66.24(Plant Sciences)We screened mutants for root growth resistance to a putative antiauxin, PCIB, which inhibits auxin action by interfering the upstream auxin signaling events. Eleven PCIB-resistant mutants were obtained. Genetic mapping indicates that the mutations are located in at least 5 independent loci including two known auxin-related loci, and . mutants (s) , and were also resistant to 2,4-D as shown by a root growth assay. Positional cloning of revealed that the gene encodes a protein with a domain of unknown function (DUF298), which has not previously been implicated in auxin signaling. The protein has a putative nuclear localization signal and shares homology with the DCN-1 protein through the DUF298 domain. The results also indicate that PCIB can facilitate the identification of factors involved in auxin or auxin-related signaling.
Rahman, A.*; Nakasone, Akari*; Chhun, T.*; Oura, Chiharu*; Biswas, K. K.*; Uchimiya, Hirofumi*; Tsurumi, Seiji*; Baskin, T. I.*; Tanaka, Atsushi; Ono, Yutaka
Plant Journal, 47(5), p.788 - 801, 2006/09
Times Cited Count:33 Percentile:60.05(Plant Sciences)2,4-D, a chemical analogue of IAA, is widely used as a growth regulator and exogenous source of auxin. It is believed that they share a common response pathway. Here, we show that a mutant, () is resistant to 2,4-D, yet nevertheless responds like the wild type to IAA. That the mutation alters 2,4-D responsiveness specifically was confirmed by analysis of GUS expression in the and backgrounds, as well as by real-time PCR quantification of expression. Complementation and RNAi experiments identified a gene that confers 2,4-D responsiveness. The gene encodes a with unknown function and present in plants, animals, and invertebrates. These results suggest that SMAP1 is a regulatory component that mediates responses to 2,4-D and that responsiveness to 2,4-D and IAA are partially distinct.
Ono, Yutaka; Rahman, A.*; Biswas, K. K.*; Chhun, T.*; Tsurumi, Seiji*; Narumi, Issei
no journal, ,
The mechanism of plant hormoneauxin action has been revealed by identification of several auxin-related mutants. However, the detailed regulatory system of signaling pathway and whether known auxin receptors TIR1/AFBs accounts for all auxin response largely remains unclear. It is may be possible that other uncharacterized proteins are involved in TIR1/AFBs dependent or independent auxin signaling pathway. To investigate novel factors involved in auxin signaling, we screened new mutants that exhibits a long primary root in presence of antiauxin PCIB. The mutants were classified at least 5 independent loci including two known auxin-related loci and . Furthermore, physiological and molecular characterization of a novel auxin-related mutants, suggested that small acidic protein 1 is a regulatory component that mediates 2,4-D-induced auxin response and mode of action of 2,4-D is distinct from that of IAA at least in part.
Ono, Yutaka; Biswas, K. K.*; Miyazaki, Yuji*; Kiyosue, Tomohiro*; Narumi, Issei
no journal, ,
We have screened Arabidopsis mutants for root growth resistance to a putative antiauxin, -chlorophenoxyisobutyric acid (PCIB). We have successfully isolated at least three novel antiauxin-resistant mutants (). The , mutant was also resistant to 2,4-D as shown by a root growth assay. The gene encodes a protein with a domain of unknown function (DUF298). The protein has a putative nuclear localization signal and its nuclear localization was confirmed by a protoplast transient assay. The protein shares homology with the DEFECTIVE IN CULLIN NEDDYLATION-1 protein through the DUF298 domain. However, no significant difference in the auxin responsive markers, or , was observed between the wild type and , suggesting that the gene regulates 2,4-D sensitivity through a previously uncharacterized mechanism.
Ono, Yutaka; Biswas, K. K.*; Nakasone, Akari; Miyazaki, Yuji*; Kiyosue, Tomohiro*; Narumi, Issei
no journal, ,
We have successfully isolated a novel mutants (), which was resistant to synthetic auxin 2,4-dichlorophenoxyacetic acid as shown by a root growth assay. Positional cloning revealed that the AAR3 gene encodes a nuclear localized protein that shares homology with the Defective in Cullin Neddylation-1 (DCN1) protein through the PONY domain. The result suggested that the Arabidopsis DCN1-like protein (AAR3) regulates responses to 2,4-dichlorophenoxyacetic acid in roots.
Ono, Yutaka; Nakasone, Akari*; Biswas, K.; Narumi, Issei
no journal, ,
no abstracts in English
Biswas, K.; Narumi, Issei; Ono, Yutaka; Mori, Takeshi*; Kogawara, Satoshi*
no journal, ,
Biswas, K.; Mori, Takeshi*; Kogawara, Satoshi*; Hase, Yoshihiro; Narumi, Issei; Ono, Yutaka
no journal, ,
Ono, Yutaka; Nakasone, Akari*; Fujiwara, Masayuki*; Fukao, Yoichiro*; Biswas, K.; Rahman, A.*; Kawai, Maki*; Uchimiya, Hirofumi*; Narumi, Issei
no journal, ,