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Klara Totpal

Researcher at Genentech

Publications -  70
Citations -  8919

Klara Totpal is an academic researcher from Genentech. The author has contributed to research in topics: Receptor & Tumor necrosis factor alpha. The author has an hindex of 38, co-authored 68 publications receiving 8103 citations. Previous affiliations of Klara Totpal include University of Texas MD Anderson Cancer Center.

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Differential hepatocyte toxicity of recombinant Apo2L/TRAIL versions

TL;DR: These findings not only provide a novel insight into the pathogenesis of the transplant-related atherosclerosis, but also point to a new therapeutic strategy that involves targeting of homing, differentiation and proliferation of putative smooth-muscle progenitor cells derived from the recipient.
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Mapping of the C1q Binding Site on Rituxan, a Chimeric Antibody with a Human IgG1 Fc

TL;DR: The results demonstrate that the previously described C1q binding motif in murine IgG2b constituting residues E318, K320, and K322 is not applicable to a human IgG1 when challenged with either human, rabbit, or guinea pig complement and suggest that there are species-specific differences in the C 1q binding site of Igs.
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Death-receptor O-glycosylation controls tumor-cell sensitivity to the proapoptotic ligand Apo2L/TRAIL

TL;DR: A new link between death-receptor O-glycosylation and apoptotic signaling is uncovered, providing potential predictive biomarkers for Apo2L/TRAIL-based cancer therapy.
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Tumor-cell resistance to death receptor–induced apoptosis through mutational inactivation of the proapoptotic Bcl-2 homolog Bax

TL;DR: It is shown that Bax mutation in mismatch repair–deficient tumors can cause resistance to death receptor–targeted therapy, but pre-exposure to chemotherapy rescues tumor sensitivity.
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Engineered Antibodies with Increased Activity to Recruit Complement

TL;DR: It is revealed that the residues K326 and E333 play a significant role in the control of the biological activity of an IgG molecule and can rescue the activity of a inactive IgG isotype.