The Sel1L-Hrd1 Endoplasmic Reticulum-Associated Degradation Complex Manages a Key Checkpoint in B Cell Development
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文摘

ERAD deficiency blocks the transition from large pre-B cells to small pre-B cells

ERAD manages a B cell developmental checkpoint by attenuating pre-BCR signaling

The pre-BCR complex is an endogenous Sel1L-Hrd1 ERAD substrate in B cells

Pre-BCR degradation by the Sel1L-Hrd1 complex requires the ER chaperone BiP

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