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0032 (0)16 41 44 07
+32 1650 9045
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fax +32 1650 9045
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tel +81 78 386 0860
fax +81 78 306 0296
Česká republika Praha
US New York
0032 (0)16 41 44 07
Recombinant Mouse Fibroblast Growth Factor-basic (FGF-basic)
(Cat. No.: C044)
FGF basic (FGF-2, HBGF-2) is one of at least 22 mitogenic proteins of the FGF family, which show 35-60% amino acid conservation. Unlike other FGFs, FGF acidic and basic lack signal peptides and are secreted by an alternate pathway. The 17 kDa mouse sequence has 98% aa identity with rat, and 95% identity with human, bovine and sheep FGF basic. Binding of FGF to heparin or cell surface HSPG is necessary for binding, dimerization and activation of tyrosine kinase FGF receptors. FGF basic binds other proteins, polysaccharides and lipids with lower affinity. Expression of FGF basic is nearly ubiquitous but disruption of the mouse FGF basic gene gives a relatively mild phenotype, suggesting compensation by other FGF family members. FGF basic modulates such normal processes as angiogenesis,
wound healing and tissue repair, embryonic development and differentiation, neuronal function and neural degeneration. Transgenic overexpression of FGF basic results in excessive proliferation and angiogenesis reminiscent of a variety of pathological conditions.
Recombinant Mouse FGF-basic produced in E. coli is a non-glycosylated polypeptide chain containing 154 amino acids and having a molecular mass of 17153 Dalton.
Biological activity: The ED50 as determined by the dose-dependant proliferation of BALB/3T3 cells was found to be less than 0.5 ng/ml, corresponding to a Specific Activity of 2.0 x 106 IU/mg.
Purity:Greater than 95% as determined by
(a) Analysis by HPLC.
(b) Analysis by reducing and non-reducing SDS-PAGE Silver Stained gel..
Amino-Acid Sequence: The sequence of the first five N-terminal amino acids was determined and was found to be Met-Ala-Ala-Ser-Gly.
Endotoxin: Less than 0.1ng/µg (1 IEU/µg) of FGF-basic.
Mouse FGF-basic was lyophilized from 1mg/ml solution after extensive dialysis against 20 mM phosphate buffer, pH 7.2, 50 mM Na2SO4, 0.2 mM DTT and 0.2 mM EDTA.
Lyophilized rmFGF-basic although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution rmFGF-basic should be stored at 4°C between 2-7 days and for future use below -18°C. For long-term storage it is recommended to add a carrier protein (0.1% HSA or BSA).
Please avoid freeze-thaw cycles.
It is recommended to reconstitute the lyophilized rmFGF-basic in sterile 18MΩ-cm H2O not less than 100µg/ml, which can then be further diluted to other aqueous solutions.
1: Ann Biol Clin (Paris) ;Vol 66(3)
[Biology and potential of human embryonic stem cells]
[Abstract] Human embryonic stem cells (hESC) are obtained from the inner cell mass from the early embryo at blastocyste stage. Derived in cell lines for the first time in 1998, they can be maintained in culture in an undifferentiated state indefinitely under certain conditions. Two essential properties characterize hESC: pluripotency and self-renewal. Pluripotency is convey by the expression of specific transcription factors such as OCT4 and NANOG, and is under the control of growth factors such as IGF2 and FGFb. Markers used to characterize these cells include surface antigens, notably SSEA-3 and SSEA-4, and nuclear markers such as OCT4. HESC can differentiate into different cell types in vitro. They represent a unique and essential model for early human development
research and for regenerative medicine. By their self-renewal capacity and their potential to differentiate into several cell types, hESC are an unlimited source of cells enabling to replace or restore lost or damaged cells in numerous diseases. Even if it is not conceivable today to use them in clinical practice for ethic and scientific reasons, it seems essential to explore the numerous potentialities of these cells. This knowledge might be relevant to handle adult stem cells in vitro and will be mandatory for a therapeutic use of hESC in the future.
2: Microb Pathog 2008 Mar;Vol 44(3)
A functional epitope of the pneumococcal surface adhesin A activates nasopharyngeal cells and increases bacterial internalization.
[Abstract] Pneumococcal surface adhesin A (PsaA) is a putative pneumococcal (Pnc) adhesin known to bind to nasopharyngeal (NP) epithelial cells. This study evaluated the effect of peptides within a functional domain of PsaA on NP cells. Detroit 562 NP cells were treated with synthetic peptides derived from PsaA (P4, P6, and P7; 28, 12, and 16 amino acids, respectively). The P4 peptide also binds to NP cells. Analysis of P4-treated NP cells by transmission electron microscopy revealed major cytological changes. Of 9 cytokines analyzed, a 6-fold increase in FGFb secretion at 3 and 6h (11-fold at 12h) was found post-P4 treatment of NP cells. There was a simultaneous reduction in the secreted levels of IL-6, IL-8, and VEGF. We observed enhancement in the adherence of Pnc
strains to P4-treated NP cells (2-38-fold increase). Enhancement in adherence (2-fold increase) to P4-treated NP cells was also recorded with other streptococcal species (Streptococcus mitis and Streptococcus pyogenes). Internalization experiments demonstrated that 45% of the adherent bacteria were actually internalized after pretreatment with P4 peptide as compared to controls. Peptide fragments of P4, P6 and P7 did not activate NP cells to the extent of P4 peptide. The P4-mediated enhancement of Pnc adherence was blocked (100%) by anti-P4 antibodies, confirming the specificity of the P4 sequence for NP cell activation. Our data suggests that this functional domain of PsaA contained within the P4 sequence binds and activates NP cells to facilitate Pnc invasion.
3: Eur Cytokine Netw 2007
Predominance of Th2 cytokines, CXC chemokines and innate immunity mediators at the mucosal level during severe respiratory syncytial virus infection in children.
[Abstract] Profiling of immune mediators in both nasal and plasma samples is a common approach to the study of pathogenesis in respiratory viral infections. Nevertheless, mucosal immunity functions essentially independently from peripheral immunity. In our study, 27 immune mediators were profiled in parallel, in nasopharyngeal aspirates (NPAs) and plasma from 22 < 2 year-old children with a severe respiratory syncytial virus infection involving the lower respiratory tract, using a multiplex assay. NPAs from 22 children with innocent heart murmurs were used as controls. Differences in mediator concentrations between NPAs from patients and controls were assessed using the Mann-Whitney test. Ratios of innate/adaptive-immunity mediators, Th2/Th1-cytokines and
CXC/CC-chemokines were calculated for NPAs and plasmas and differences were assessed using the Wilcoxon test. Associations mediators, severity and leukocyte counts were studied using the Spearman-Karber test. Results: increased levels of Th1 cytokines (IL-1beta, IL-2, IL-12p70, IFNgamma, TNFalpha), Th2 cytokines (IL-13, IL-4, IL-6, IL-10), chemokines (IP-10, IL-8, MIP1alpha, MIP-1beta), growth factors (FGFb, PDGFbb, GCSF) and IL-1RA, IL-17 were observed in patient NPAs in comparison to controls. In the relative comparisons between patient NPAs and plasmas, a predominance of innate immunity mediators, Th2 cytokines and CXC chemokines was found at the mucosal level. No association between the level of each mediator in NPAs and plasma was found. In plasma, PDGFbb, VEGF, MIP-1alpha, IL-8
correlated with severity; RANTES and IL-6 correlated with leukocyte counts. Conclusions: acute respiratory syncytial virus infection induces a relative predominance of innate-immunity mediators, Th2 cytokines and CXC chemokines in the mucosal compartment in infected children.
4: J Cell Physiol 2007
Reduced chondrogenic potential of adipose tissue derived stromal cells correlates with an altered TGFbeta receptor and BMP profile and is overcome by BMP-6.
[Abstract] Recent interest has focused on mesenchymal stem cells (MSC) for tissue engineering and regenerative therapy of cartilage defects. MSC originating from adipose tissue (ATSC) are attractive as they are easily available and abundant. They have similar properties like bone marrow derived MSC (BMSC), except for a reduced chondrogenic potential under standard culture conditions driven by TGFbeta. Aim of this study was to search for possible differences explaining the reduced differentiation capacity of ATSC and to eliminate it by adaptation of induction protocols. Expanded MSC were analyzed for their growth factor and related receptor repertoire and ATSC spheroid cultures were supplemented with BMP-2,-4,-6,-7, TGFbeta, FGFa, FGFb, IGF-1, and PTHrP alone or in
combination with TGFbeta. In contrast to BMSC, ATSC showed reduced expression of BMP-2, -4, and -6 mRNA and did not express TGFbeta-receptor-I protein. Consistent with this, increased concentrations of TGFbeta did not improve chondrogenesis of ATSC. BMP6 treatment induced TGFbeta-receptor-I expression and combined application of TGFbeta and BMP-6 eliminated the reduced chondrogenic potential of ATSC inducing a gene expression profile similar to differentiated BMSC. Like in BMSC, chondrogenesis of ATSC was associated with hypertrophy according to premature collagen Type X expression, upregulation of alkaline-phosphatase activity and in vivo calcification of spheroids after ectopic transplantation in SCID mice. In conclusion, a distinct BMP and TGFbeta-receptor repertoire may explain the
reduced chondrogenic capacity of ATSC in vitro, which could be compensated by exogenous application of lacking factors. Further studies should now be directed to induce chondrogenesis in the absence of hypertrophy.
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