Biochemical and Biophysical Research Communications (BIOCHEM BIOPH RES CO)
Biochemical and Biophysical Research Communications is the premier international journal devoted to the very rapid dissemination (six weeks) of timely and significant experimental results in the diverse fields of biological research. Frequent publication (36 issues per year) ensures a steady stream of information. The development of the "Breakthroughs and Views" section brings the minireview format to the journal. In addition, the editors have expanded the journalís scope. Research Areas now include: Biochemistry Cell Biology; Developmental Biology; Immunology; Neurobiology; Biophysics; Molecular Biology; Plant Biology.
- Impact factor2.48Show impact factor historyHide impact factor history
- WebsiteBiochemical and Biophysical Research Communications website
Other titlesBiochemical and biophysical research communications, BBRC
Material typePeriodical, Internet resource
Document typeJournal / Magazine / Newspaper, Internet Resource
- Author can archive a pre-print version
- Author can archive a post-print version
- Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
- Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
- Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
- Set statement to accompany deposit
- Published source must be acknowledged
- Must link to journal home page or articles' DOI
- Publisher's version/PDF cannot be used
- Articles in some journals can be made Open Access on payment of additional charge
- NIH Authors articles will be submitted to PMC after 12 months
- Authors who are required to deposit in subject repositories may also use Sponsorship Option
- Pre-print can not be deposited for The Lancet
Publications in this journal
Biochemical and Biophysical Research Communications 03/2013;
[show abstract] [hide abstract]
ABSTRACT: Lifestyle-related diseases are increasing and the challenge to create innovative drugs to treat such diseases is a main focus in medical science research. Fibroblast growth factor 21 (FGF21) is a powerful modulator of glucose and lipid metabolism, and is an innovative candidate drug already in clinical trials for type 2 diabetes mellitus and obesity. Bone fragility and impaired fracture healing induced by such lifestyle-related conditions are also a growing problem. Bone morphogenic proteins (BMPs) are well known osteogenic growth factors, and BMP-2 is used to augment bone formation in difficult clinical situations. There are many documented interactions between the FGF and BMP family proteins, although the interaction between FGF21 and BMP-2 remains unknown. The aim of this study was to reveal the effect of FGF21 toward BMP-2-dependent osteogenic activity, using C2C12 cells as a model system. We found that FGF21 enhanced BMP-2-dependent transcription and osteogenesis in the C2C12 cell line, which was confirmed by alkaline phosphatase activity, matrix mineralization, and gene expression. Mechanistically, FGF21 enhanced BMP-2-induced intracellular signaling through Smad proteins, but not through p44/42MAPK proteins. Furthermore, we identified a negative feedback loop in which BMP-2 decreased endogenous FGF21 mRNA expression. In summary, this study demonstrates interactions between BMP-2 and FGF21 pathways exist in vitro, and that FGF21 enhances the osteogenic activity of BMP-2 by up-regulating the BMP-2-dependent Smad signaling pathway.Biochemical and Biophysical Research Communications 02/2013;
Article: Enhancement of production of eugenol and its glycosides in transgenic aspen plants via genetic engineeringBiochemical and Biophysical Research Communications 01/2013;
Article: Evolutionary landscape of amphibians emerging from ancient freshwater fish inferred from complete mitochondrial genomesBiochemical and Biophysical Research Communications 01/2012;
Biochemical and Biophysical Research Communications 01/2012; http://dx.doi.org/10.1016/j.bbrc.2012.06.012.
Article: Evaluation of anti-depressant-like activity of linezolid, an oxazolidinone class derivative – An investigation using behavioral tests battery of depressionBiochemical and Biophysical Research Communications 05/2011;
Article: Reduced expression and abnormal localization of the K(ATP) channel subunit SUR2A in patients with familial hypokalemic periodic paralysis.[show abstract] [hide abstract]
ABSTRACT: Familial hypokalemic periodic paralysis is an autosomal-dominant channelopathy that features episodic attacks of flaccid paralysis with concomitant hypokalemia. Reduced activity of ATP-sensitive K+ (KATP) channels is suggested to be responsible for this disorder; however, the molecular mechanisms have not yet been elucidated. In this study, we investigated the molecular mechanism of reduced KATP channel activity in skeletal muscle cells of patients with familial hypokalemic periodic paralysis. We examined the mRNA and protein levels of SUR2A, a KATP channel subunit, in cells from patients (patient cells) and normal individuals (normal cells). Our results demonstrated that normal cells exposed to 50 mM potassium buffer, which was used to induce depolarization, did not show significant change in the SUR2A mRNA levels; however, the protein level significantly increased in the cytosolic fraction. When the patient cells were exposed to 50 mM potassium buffer, the SUR2A mRNA level significantly decreased. Further, the protein level of SUR2A significantly increased in the membrane fraction but decreased in the cytosolic fraction in patient cells. These findings suggest that abnormal localization of the SUR2A K+ channel protein leads to reduced KATP channel activity in familial hypokalemic periodic paralysis.Biochemical and Biophysical Research Communications 01/2010; 391(1):974-978.
Article: In vitro differentiation of retinal ganglion-like cells from embryonic stem cell derived neural progenitors[show abstract] [hide abstract]
ABSTRACT: ES cells have been reported to serve as an excellent source for obtaining various specialized cell types and could be used in cell replacement therapy. Here, we demonstrate the potential of ES cells to differentiate along retinal ganglion cell (RGC) lineage. FGF2-induced ES cell derived neural progenitors (ES-NPs) were able to generate RGC-like cells in vitro upon differentiation. These cells expressed RGC regulators and markers such as, Ath5, Brn3b, RPF-1, Thy-1 and Islet-1, confirming their potential to differentiate into RGCs. The generation of RGCs from ES-NPs was enhanced with the exposure of FGF2 and Sonic hedgehog (Shh), although Shh treatment alone did not affect RGC differentiation significantly. ES-NPs, after exposure to FGF2, were capable of integrating and differentiating into RGCs in vivo upon transplantation. Thus, our study suggests that ES cells can serve an excellent renewable source for generating RGCs that can be used to treat neurodegenerative diseases like glaucomaBiochemical and Biophysical Research Communications 03/2009; 380(2):230-235.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
ISSN: 1995-7645, Impact factor: 0.37
ISSN: 1949-2553, Impact factor: 4.78
Endocrine Society; HighWire Press
ISSN: 1945-7170, Impact factor: 4.46
European Societies of Toxicology,...
ISSN: 1879-3169, Impact factor: 3.23
ISSN: 1879-0712, Impact factor: 2.59
ISSN: 1879-0631, Impact factor: 2.56
Bentham Science Publishers
ISSN: 1873-5576, Impact factor: 5.13