The Ca2+-binding endoplasmic reticulum protein STIM1 was discovered to be pivotal for mast cell function. Yoshihiro Baba and colleagues from the RIKEN Research Center for Allergy and Immunology in Japan observed fetal liver-derived mast cells with defective STIM1 and found out that they had impaired Ca2+ influx due to high-affinity immunoglobulin E receptor FcεRI and activation of the transcription factors NF-κB and NFAT. Those mast cells also showed reduced degranulation and cytokine production after FcεRI stimulation.

Mast cells act as effectors of allergic inflammatory diseases, mediated by immunoglobulin E. The inflammatory mediators are secreted by mast cells upon stimulation by Ca2+ influx. Experiments showed that alterations in STIM1 expression affected the sensitivity of immunoglobulin E-mediated immediate-phase anaphylactic responses in vivo.

Apparently STIM1 promotes Ca2+ influx, thus controlling mast cell activation and anaphylaxis through FcεRI.

Related antibodies on antibodies-online.com:

Mast cells

STIM1 (stromal interaction molecule 1)

Immunoglobulin E

NF-κB

NFAT

FcεRI

NFAT1

NFAT2

NFAT3

NFAT5

Fc fragment of IgE, FCE1A, FcERI

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Antibodies for the research area inflammation: »Show antibodies