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Showing 25 to 36 of 3935 entries
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Some Changes in Submission and Handling Policies at the JBC.

The Journal of biological chemistry

[No authors listed]
PMID: 26567297
J Biol Chem. 2015 Nov 13;290(46):28018-9. doi: 10.1074/jbc.E115.000001.

No abstract available.

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Some Changes in Submission and Handling Policies at the JBC. J Biol Chem. 2015;290(46):28018-9doi: 10.1074/jbc.E115.000001.
(2015). Some Changes in Submission and Handling Policies at the JBC. The Journal of biological chemistry, 290(46), 28018-9. https://doi.org/10.1074/jbc.E115.000001
"Some Changes in Submission and Handling Policies at the JBC." The Journal of biological chemistry vol. 290,46 (2015): 28018-9. doi: https://doi.org/10.1074/jbc.E115.000001
Some Changes in Submission and Handling Policies at the JBC. J Biol Chem. 2015 Nov 13;290(46):28018-9. doi: 10.1074/jbc.E115.000001. PMID: 26567297; PMCID: PMC4646039.
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Site-directed mutagenesis reveals regions implicated in the stability and fiber formation of human λ3r light chains.

The Journal of biological chemistry

Villalba MI, Canul-Tec JC, Luna-Martínez OD, Sánchez-Alcalá R, Olamendi-Portugal T, Rudiño-Piñera E, Rojas S, Sánchez-López R, Fernández-Velasco DA, Becerril B.
PMID: 26002949
J Biol Chem. 2015 May 22;290(21):13039. doi: 10.1074/jbc.A114.629550.

No abstract available.

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Villalba MI, Canul-Tec JC, Luna-Martínez OD, et al. Site-directed mutagenesis reveals regions implicated in the stability and fiber formation of human λ3r light chains. J Biol Chem. 2015;290(21):13039doi: 10.1074/jbc.A114.629550.
Villalba, M. I., Canul-Tec, J. C., Luna-Martínez, O. D., Sánchez-Alcalá, R., Olamendi-Portugal, T., Rudiño-Piñera, E., Rojas, S., Sánchez-López, R., Fernández-Velasco, D. A., & Becerril, B. (2015). Site-directed mutagenesis reveals regions implicated in the stability and fiber formation of human λ3r light chains. The Journal of biological chemistry, 290(21), 13039. https://doi.org/10.1074/jbc.A114.629550
Villalba, Miryam I, et al. "Site-directed mutagenesis reveals regions implicated in the stability and fiber formation of human λ3r light chains." The Journal of biological chemistry vol. 290,21 (2015): 13039. doi: https://doi.org/10.1074/jbc.A114.629550
Villalba MI, Canul-Tec JC, Luna-Martínez OD, Sánchez-Alcalá R, Olamendi-Portugal T, Rudiño-Piñera E, Rojas S, Sánchez-López R, Fernández-Velasco DA, Becerril B. Site-directed mutagenesis reveals regions implicated in the stability and fiber formation of human λ3r light chains. J Biol Chem. 2015 May 22;290(21):13039. doi: 10.1074/jbc.A114.629550. PMID: 26002949; PMCID: PMC4505558.
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Differential expression of intracellular and secreted osteopontin isoforms by murine macrophages in response to Toll-like receptor agonists.

The Journal of biological chemistry

[No authors listed]
PMID: 26002950
J Biol Chem. 2015 May 22;290(21):13040. doi: 10.1074/jbc.A110.110312.

No abstract available.

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Differential expression of intracellular and secreted osteopontin isoforms by murine macrophages in response to Toll-like receptor agonists. J Biol Chem. 2015;290(21):13040doi: 10.1074/jbc.A110.110312.
(2015). Differential expression of intracellular and secreted osteopontin isoforms by murine macrophages in response to Toll-like receptor agonists. The Journal of biological chemistry, 290(21), 13040. https://doi.org/10.1074/jbc.A110.110312
"Differential expression of intracellular and secreted osteopontin isoforms by murine macrophages in response to Toll-like receptor agonists." The Journal of biological chemistry vol. 290,21 (2015): 13040. doi: https://doi.org/10.1074/jbc.A110.110312
Differential expression of intracellular and secreted osteopontin isoforms by murine macrophages in response to Toll-like receptor agonists. J Biol Chem. 2015 May 22;290(21):13040. doi: 10.1074/jbc.A110.110312. PMID: 26002950; PMCID: PMC4505559.
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WITHDRAWN: A mutation in the chaperone σ1-receptor impairs mitochondrial ATP production in amyotrophic lateral sclerosis.

The Journal of biological chemistry

Tagashira H, Shioda N, Fukunaga K.
PMID: 24338012
J Biol Chem. 2014 Jan 07; doi: 10.1074/jbc.M113.499442. Epub 2014 Jan 07.

This manuscript was withdrawn by the Author.

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Tagashira H, Shioda N, Fukunaga K. WITHDRAWN: A mutation in the chaperone σ1-receptor impairs mitochondrial ATP production in amyotrophic lateral sclerosis. J Biol Chem. 2014;doi: 10.1074/jbc.M113.499442.
Tagashira, H., Shioda, N., & Fukunaga, K. (2014). WITHDRAWN: A mutation in the chaperone σ1-receptor impairs mitochondrial ATP production in amyotrophic lateral sclerosis. The Journal of biological chemistry, . https://doi.org/10.1074/jbc.M113.499442
Tagashira, Hideaki, et al. "WITHDRAWN: A mutation in the chaperone σ1-receptor impairs mitochondrial ATP production in amyotrophic lateral sclerosis." The Journal of biological chemistry vol. (2014). doi: https://doi.org/10.1074/jbc.M113.499442
Tagashira H, Shioda N, Fukunaga K. WITHDRAWN: A mutation in the chaperone σ1-receptor impairs mitochondrial ATP production in amyotrophic lateral sclerosis. J Biol Chem. 2014 Jan 07; doi: 10.1074/jbc.M113.499442. Epub 2014 Jan 07. PMID: 24338012.
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14-3-3ϵ and 14-3-3σ inhibit Toll-like receptor (TLR)-mediated proinflammatory cytokine induction.

The Journal of biological chemistry

[No authors listed]
PMID: 25217707
J Biol Chem. 2014 Sep 12;289(37):25474. doi: 10.1074/jbc.A112.367490.

No abstract available.

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14-3-3ϵ and 14-3-3σ inhibit Toll-like receptor (TLR)-mediated proinflammatory cytokine induction. J Biol Chem. 2014;289(37):25474doi: 10.1074/jbc.A112.367490.
(2014). 14-3-3ϵ and 14-3-3σ inhibit Toll-like receptor (TLR)-mediated proinflammatory cytokine induction. The Journal of biological chemistry, 289(37), 25474. https://doi.org/10.1074/jbc.A112.367490
"14-3-3ϵ and 14-3-3σ inhibit Toll-like receptor (TLR)-mediated proinflammatory cytokine induction." The Journal of biological chemistry vol. 289,37 (2014): 25474. doi: https://doi.org/10.1074/jbc.A112.367490
14-3-3ϵ and 14-3-3σ inhibit Toll-like receptor (TLR)-mediated proinflammatory cytokine induction. J Biol Chem. 2014 Sep 12;289(37):25474. doi: 10.1074/jbc.A112.367490. PMID: 25217707; PMCID: PMC4162152.
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Characterization of a novel β-L-arabinofuranosidase in Bifidobacterium longum. Functional elucidation of a DUF1680 family member.

The Journal of biological chemistry

Fujita K, Takashi Y, Obuchi E, Kitahara K, Suganuma T.
PMID: 24143008
J Biol Chem. 2013 Oct 18;288(42):30502. doi: 10.1074/jbc.A111.248690.

No abstract available.

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Fujita K, Takashi Y, Obuchi E, et al. Characterization of a novel β-L-arabinofuranosidase in Bifidobacterium longum. Functional elucidation of a DUF1680 family member. J Biol Chem. 2013;288(42):30502doi: 10.1074/jbc.A111.248690.
Fujita, K., Takashi, Y., Obuchi, E., Kitahara, K., & Suganuma, T. (2013). Characterization of a novel β-L-arabinofuranosidase in Bifidobacterium longum. Functional elucidation of a DUF1680 family member. The Journal of biological chemistry, 288(42), 30502. https://doi.org/10.1074/jbc.A111.248690
Fujita, Kiyotaka, et al. "Characterization of a novel β-L-arabinofuranosidase in Bifidobacterium longum. Functional elucidation of a DUF1680 family member." The Journal of biological chemistry vol. 288,42 (2013): 30502. doi: https://doi.org/10.1074/jbc.A111.248690
Fujita K, Takashi Y, Obuchi E, Kitahara K, Suganuma T. Characterization of a novel β-L-arabinofuranosidase in Bifidobacterium longum. Functional elucidation of a DUF1680 family member. J Biol Chem. 2013 Oct 18;288(42):30502. doi: 10.1074/jbc.A111.248690. PMID: 24143008; PMCID: PMC3798514.
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MicroRNAs as mediators of cardiovascular disease: Targets to be manipulated.

World journal of biological chemistry

Lee S, Choi E, Kim SM, Hwang KC.
PMID: 26009702
World J Biol Chem. 2015 May 26;6(2):34-8. doi: 10.4331/wjbc.v6.i2.34.

Cardiovascular disease has been the leading cause of death worldwide for the last few decades. Even with the rapid progression of the biomedical field, conquering/managing cardiovascular disease is not an easy task because it is multifactorial disease. One of...

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Lee S, Choi E, Kim SM, et al. MicroRNAs as mediators of cardiovascular disease: Targets to be manipulated. World J Biol Chem. 2015;6(2):34-8doi: 10.4331/wjbc.v6.i2.34.
Lee, S., Choi, E., Kim, S. M., & Hwang, K. C. (2015). MicroRNAs as mediators of cardiovascular disease: Targets to be manipulated. World journal of biological chemistry, 6(2), 34-8. https://doi.org/10.4331/wjbc.v6.i2.34
Lee, Seahyoung, et al. "MicroRNAs as mediators of cardiovascular disease: Targets to be manipulated." World journal of biological chemistry vol. 6,2 (2015): 34-8. doi: https://doi.org/10.4331/wjbc.v6.i2.34
Lee S, Choi E, Kim SM, Hwang KC. MicroRNAs as mediators of cardiovascular disease: Targets to be manipulated. World J Biol Chem. 2015 May 26;6(2):34-8. doi: 10.4331/wjbc.v6.i2.34. PMID: 26009702; PMCID: PMC4436904.
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NMR-based structural analysis of the complete rough-type lipopolysaccharide isolated from Capnocytophaga canimorsus.

The Journal of biological chemistry

Zähringer U, Ittig S, Lindner B, Moll H, Schombel U, Gisch N, Cornelis GR.
PMID: 26475523
J Biol Chem. 2015 Oct 16;290(42):25273. doi: 10.1074/jbc.A114.571489.

No abstract available.

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Zähringer U, Ittig S, Lindner B, et al. NMR-based structural analysis of the complete rough-type lipopolysaccharide isolated from Capnocytophaga canimorsus. J Biol Chem. 2015;290(42):25273doi: 10.1074/jbc.A114.571489.
Zähringer, U., Ittig, S., Lindner, B., Moll, H., Schombel, U., Gisch, N., & Cornelis, G. R. (2015). NMR-based structural analysis of the complete rough-type lipopolysaccharide isolated from Capnocytophaga canimorsus. The Journal of biological chemistry, 290(42), 25273. https://doi.org/10.1074/jbc.A114.571489
Zähringer, Ulrich, et al. "NMR-based structural analysis of the complete rough-type lipopolysaccharide isolated from Capnocytophaga canimorsus." The Journal of biological chemistry vol. 290,42 (2015): 25273. doi: https://doi.org/10.1074/jbc.A114.571489
Zähringer U, Ittig S, Lindner B, Moll H, Schombel U, Gisch N, Cornelis GR. NMR-based structural analysis of the complete rough-type lipopolysaccharide isolated from Capnocytophaga canimorsus. J Biol Chem. 2015 Oct 16;290(42):25273. doi: 10.1074/jbc.A114.571489. PMID: 26475523; PMCID: PMC4646177.
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Hierarchal autophagic divergence of hematopoietic system.

The Journal of biological chemistry

Cao Y, Zhang S, Yuan N, Wang J, Li X, Xu F, Lin W, Song L, Fang Y, Wang Z, Wang Z, Zhang H, Zhang Y, Zhao W, Hu S, Zhang X, Wang J.
PMID: 26637666
J Biol Chem. 2015 Dec 04;290(49):29240. doi: 10.1074/jbc.A115.650028.

No abstract available.

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Cao Y, Zhang S, Yuan N, et al. Hierarchal autophagic divergence of hematopoietic system. J Biol Chem. 2015;290(49):29240doi: 10.1074/jbc.A115.650028.
Cao, Y., Zhang, S., Yuan, N., Wang, J., Li, X., Xu, F., Lin, W., Song, L., Fang, Y., Wang, Z., Wang, Z., Zhang, H., Zhang, Y., Zhao, W., Hu, S., Zhang, X., & Wang, J. (2015). Hierarchal autophagic divergence of hematopoietic system. The Journal of biological chemistry, 290(49), 29240. https://doi.org/10.1074/jbc.A115.650028
Cao, Yan, et al. "Hierarchal autophagic divergence of hematopoietic system." The Journal of biological chemistry vol. 290,49 (2015): 29240. doi: https://doi.org/10.1074/jbc.A115.650028
Cao Y, Zhang S, Yuan N, Wang J, Li X, Xu F, Lin W, Song L, Fang Y, Wang Z, Wang Z, Zhang H, Zhang Y, Zhao W, Hu S, Zhang X, Wang J. Hierarchal autophagic divergence of hematopoietic system. J Biol Chem. 2015 Dec 04;290(49):29240. doi: 10.1074/jbc.A115.650028. PMID: 26637666; PMCID: PMC4705929.
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Translocation of heme oxygenase-1 to mitochondria is a novel cytoprotective mechanism against non-steroidal anti-inflammatory drug-induced mitochondrial oxidative stress, apoptosis, and gastric mucosal injury.

The Journal of biological chemistry

Bindu S, Pal C, Dey S, Goyal M, Alam A, Iqbal MS, Dutta S, Sarkar S, Kumar R, Maity P, Bandyopadhyay U.
PMID: 26025999
J Biol Chem. 2015 May 29;290(22):13667-8. doi: 10.1074/jbc.A111.279893.

No abstract available.

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Bindu S, Pal C, Dey S, et al. Translocation of heme oxygenase-1 to mitochondria is a novel cytoprotective mechanism against non-steroidal anti-inflammatory drug-induced mitochondrial oxidative stress, apoptosis, and gastric mucosal injury. J Biol Chem. 2015;290(22):13667-8doi: 10.1074/jbc.A111.279893.
Bindu, S., Pal, C., Dey, S., Goyal, M., Alam, A., Iqbal, M. S., Dutta, S., Sarkar, S., Kumar, R., Maity, P., & Bandyopadhyay, U. (2015). Translocation of heme oxygenase-1 to mitochondria is a novel cytoprotective mechanism against non-steroidal anti-inflammatory drug-induced mitochondrial oxidative stress, apoptosis, and gastric mucosal injury. The Journal of biological chemistry, 290(22), 13667-8. https://doi.org/10.1074/jbc.A111.279893
Bindu, Samik, et al. "Translocation of heme oxygenase-1 to mitochondria is a novel cytoprotective mechanism against non-steroidal anti-inflammatory drug-induced mitochondrial oxidative stress, apoptosis, and gastric mucosal injury." The Journal of biological chemistry vol. 290,22 (2015): 13667-8. doi: https://doi.org/10.1074/jbc.A111.279893
Bindu S, Pal C, Dey S, Goyal M, Alam A, Iqbal MS, Dutta S, Sarkar S, Kumar R, Maity P, Bandyopadhyay U. Translocation of heme oxygenase-1 to mitochondria is a novel cytoprotective mechanism against non-steroidal anti-inflammatory drug-induced mitochondrial oxidative stress, apoptosis, and gastric mucosal injury. J Biol Chem. 2015 May 29;290(22):13667-8. doi: 10.1074/jbc.A111.279893. PMID: 26025999; PMCID: PMC4447946.
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Novel human homologues of p47phox and p67phox participate in activation of superoxide-producing NADPH oxidases.

The Journal of biological chemistry

Takeya R, Ueno N, Kami K, Taura M, Kohjima M, Izaki T, Nunoi H, Sumimoto H.
PMID: 25750260
J Biol Chem. 2015 Mar 06;290(10):6003. doi: 10.1074/jbc.A114.212856.

No abstract available.

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Takeya R, Ueno N, Kami K, et al. Novel human homologues of p47phox and p67phox participate in activation of superoxide-producing NADPH oxidases. J Biol Chem. 2015;290(10):6003doi: 10.1074/jbc.A114.212856.
Takeya, R., Ueno, N., Kami, K., Taura, M., Kohjima, M., Izaki, T., Nunoi, H., & Sumimoto, H. (2015). Novel human homologues of p47phox and p67phox participate in activation of superoxide-producing NADPH oxidases. The Journal of biological chemistry, 290(10), 6003. https://doi.org/10.1074/jbc.A114.212856
Takeya, Ryu, et al. "Novel human homologues of p47phox and p67phox participate in activation of superoxide-producing NADPH oxidases." The Journal of biological chemistry vol. 290,10 (2015): 6003. doi: https://doi.org/10.1074/jbc.A114.212856
Takeya R, Ueno N, Kami K, Taura M, Kohjima M, Izaki T, Nunoi H, Sumimoto H. Novel human homologues of p47phox and p67phox participate in activation of superoxide-producing NADPH oxidases. J Biol Chem. 2015 Mar 06;290(10):6003. doi: 10.1074/jbc.A114.212856. PMID: 25750260; PMCID: PMC4358237.
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Dopamine Transporter Activity Is Modulated by α-synuclein.

The Journal of biological chemistry

Butler B, Goodwin S, Saha K, Becker J, Sambo D, Davari P, Khoshbouei H.
PMID: 26048988
J Biol Chem. 2015 Jun 05; doi: 10.1074/jbc.M115.639880. Epub 2015 Jun 05.

The duration and strength of the dopaminergic signal is regulated by the dopamine transporter (DAT). Drug addiction, neurodegenerative and neuropsychiatric diseases have all been associated with altered DAT activity. The membrane localization and the activity of DAT are regulated...

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Butler B, Goodwin S, Saha K, et al. Dopamine Transporter Activity Is Modulated by α-synuclein. J Biol Chem. 2015;doi: 10.1074/jbc.M115.639880.
Butler, B., Goodwin, S., Saha, K., Becker, J., Sambo, D., Davari, P., & Khoshbouei, H. (2015). Dopamine Transporter Activity Is Modulated by α-synuclein. The Journal of biological chemistry, . https://doi.org/10.1074/jbc.M115.639880
Butler, Brittany, et al. "Dopamine Transporter Activity Is Modulated by α-synuclein." The Journal of biological chemistry vol. (2015). doi: https://doi.org/10.1074/jbc.M115.639880
Butler B, Goodwin S, Saha K, Becker J, Sambo D, Davari P, Khoshbouei H. Dopamine Transporter Activity Is Modulated by α-synuclein. J Biol Chem. 2015 Jun 05; doi: 10.1074/jbc.M115.639880. Epub 2015 Jun 05. PMID: 26048988.
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Showing 25 to 36 of 3935 entries