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Sendoa Tajada

Researcher at University of California, Davis

Publications -  16
Citations -  825

Sendoa Tajada is an academic researcher from University of California, Davis. The author has contributed to research in topics: Voltage-dependent calcium channel & Transient receptor potential channel. The author has an hindex of 11, co-authored 15 publications receiving 607 citations. Previous affiliations of Sendoa Tajada include Spanish National Research Council.

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TRPA1 channels mediate acute neurogenic inflammation and pain produced by bacterial endotoxins

TL;DR: This work shows that LPS exerts fast, membrane delimited, excitatory actions via TRPA1, a transient receptor potential cation channel that is critical for transducing environmental irritant stimuli into nociceptor activity, and finds that pain and acute vascular reactions, including neurogenic inflammation (CGRP release) caused by LPS are primarily dependent onTRPA1 channel activation in nocICEptive sensory neurons, and develop independently of TLR4 activation.
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Kv1.3 Channels Can Modulate Cell Proliferation During Phenotypic Switch by an Ion-Flux Independent Mechanism

TL;DR: These findings suggest that the signaling cascade linking Kv1.3 functional expression to cell proliferation is activated by the voltage-dependent conformational change of the channels without needing ion conduction.
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Ca2+ entry into neurons is facilitated by cooperative gating of clustered CaV1.3 channels

TL;DR: It is proposed that cooperative gating of CaV1.3S channels represents a mechanism for the regulation of Ca2+ signaling and electrical activity, leading to increased firing rates in rat hippocampal neurons.
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Calcium Permeable Channels in Cancer Hallmarks.

TL;DR: This review focuses in the role of calcium permeable channels signaling in cancer with special attention to the mechanisms behind the remodeling of the calcium signals.
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BIN1 Induces the Formation of T-Tubules and Adult-Like Ca2+ Release Units in Developing Cardiomyocytes.

TL;DR: It is shown that the role of BIN1 during the differentiation of hESC‐CMs is also important for CaV1.2 channel clustering, junctional SR organization, and the establishment of excitation–contraction coupling.