Rat IgG1 Kappa Isotype Control Antibody (Low Endotoxin, Azide-Free) (DAG-IC272) Functional Grade

Rat IgG1 Kappa Isotype Control Antibody (Low Endotoxin, Azide-Free) for FC, ELISA, FLISA, IHC, Blocking, Control

Additional Formats Available

Specifications


Host Species
Rat
Antibody Isotype
IgG1, κ
Clone
LMI/H2-3-3
Species Reactivity
N/A
Conjugate
Functional Grade

Applications


Application Notes
FC, ELISA, FLISA, IHC, Blocking, Control
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

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References


Human filarial proteins attenuate chronic colitis in an experimental mouse model

PARASITE IMMUNOLOGY

Authors: Togre, N.; Bhoj, P.; Goswami, K.; Tarnekar, A.; Patil, M.; Shende, M.

Encouraged by our earlier results of promising therapeutic effect of filarial recombinant proteins BmALT2, BmCys and WbL2 individually in the mouse model of acute ulcerative colitis, in this study, these proteins have been explored individually and in different combinations for their therapeutic potential in dextran sulphate sodium (DSS)-induced chronic colitis mice. These mice, treated with filarial proteins, showed reduced disease parameters including body weight loss, disease activity index, macroscopic and histopathological scores of colon and myeloperoxidase activity in colonic mucosa. Among various treatment schemes, rBmALT2+rBmCys which showed most pronounced therapeutic implication was found to downregulate the mRNA expressions of IFN- and TNF- and upregulate IL-10 and TGF- expression in the splenocytes. Also, increase in level of IgG1 and IgG2a isotypes in the sera of rBmALT2+rBmCys-treated colitis mice was noted. Activated NF-B level was found to be reduced in the colon of treated colitis mice compared to untreated one. In conclusion, filarial proteins in combination have been shown to improve the clinicopathologic status of chronic colitis through suppression of pro-inflammatory immune response most possibly in NF-B-dependent manner. We propose this therapeutic strategy to be tested further to be considered as an effective option in chronic colitis.

The anti-CD20 mAb LFB-R603 interrupts the dysregulated NF-kappa B/Snail/RKIP/PTEN resistance loop in B-NHL cells: Role in sensitization to TRAIL apoptosis

INTERNATIONAL JOURNAL OF ONCOLOGY

Authors: Baritaki, Stavroula; Militello, Loredana; Malaponte, Graziella; Spandidos, Demetrios A.; Salcedo, Margarita; Bonavida, Benjamin

LFB-R603 is a chimeric anti-CD20 mouse/human monoclonal antibody with a human IgG1 constant (Fe) region. In comparison to rituximab, LFB-R603 exhibits a high affinity to the Fcy RIII (CD16) and a potent in vitro antibody-dependent cellular cytotoxicity (ADCC). We examined several experimental designs for the biological anti-tumor activity of LFB-R603 as well as its sensitizing activity to apoptosis in resistant non-Hodgin's B-cell lymphoma (B-NHL) in comparison to rituximab. Treatment of the B-NHL cell line Ramos with LFB-R603 was not toxic at the concentrations used and induced cell aggregation following culture at 24 and 48 h similarly to rituximab. Hence, we hypothesized that LFB-R603 may signal the tumor cells and modify intracellular survival/anti-apoptotic pathways. Treatment of Ramos cells with LFB-R603 inhibited the constitutively active NF-kappa B survival pathway, followed by significant potentiation of TRAIL-mediated apoptosis. We examined the underlying molecular mechanism by which the LFB-R603-mediated NF-kappa B inhibition results in the reversal of tumor cell resistance to TRAIL. We hypothesized that downstream gene products regulated by NF-kappa B that are involved in the resistance may be involved in LFB-R603-mediated sensitization. We found that LFB-R603 inhibited NF-kappa B activation and the anti-apoptotic factor Snail and induced the pro-apoptotic factor RKIP. The direct roles of Snail and RKIP modulation by LFB-R603 in the reversal of B-NHL resistance to TRAIL were examined by knocking down Snail and overexpressing RKIP in Ramos cells, respectively. Both approaches increased significantly the cell sensitivity to TRAIL apoptosis. In addition to changes observed in the expression levels of Snail and RKIP, Ramos cells treated with LFB-R603 induced the expression of PTEN along with inhibition of the PI3K-AKT activated pathway. PTEN silencing in Ramos cells pretreated with LFB-R603 and TRAIL inhibited TRAIL apoptosis; thus, demonstrating that PTEN induction by LFB-R603 has a direct role in tumor cell sensitization to TRAIL apoptosis. Several of the findings obtained in the experimental designs with LFB-R603 were superior to those obtained with rituximab. Overall, the findings demonstrate that LFB-R603 interferes with the dysregulated NF-kappa B/Snail/RKIP/PTEN/AKT resistance circuitry in B-NHL cells. Further, the findings suggest that LFB-R603 may sensitize tumor cells to various apoptotic stimuli including cytotoxic ligands such as TRAIL and chemotherapeutic drugs.

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