1 ulant was decreased 2-fold within 2 hours of hypotonic shock.

2 cyt) response of Saccharomyces cerevisiae to hypotonic shock.

3    We depleted peritoneal B cells in mice by hypotonic shock.

4 ase cascade are critical for the response to hypotonic shock.

5 sin D, by K(+)-depletion in combination with hypotonic shock, and by mutation of the protein kinase A

6 , we locally depleted peritoneal B cells via hypotonic shock before disease induction.

7  found in many bacteria, protects cells from hypotonic shock by reducing intracellular pressure throu

8 how a swelling-induced Cl- current following hypotonic shock, by recording membrane current responses

9                         These data show that hypotonic shock generates a stretch-activated channel-de

10           Inhibition of protein synthesis by hypotonic shock has not been reported previously.

11                      However, treatment with hypotonic shock or EGTA transiently increased transepith

12 tes that animal cells, in response to either hypotonic shock or ER stress, can bypass the cholesterol

13                     Results obtained using a hypotonic shock should, therefore, be viewed with cautio

14                                Minutes after hypotonic shock, srp-6 null animals underwent a catastro

15                                   Faced with hypotonic shock, to circumvent cell lysis, bacteria open

16 lly delivered into the macrophage cytosol by hypotonic shock treatment, indicating that ESX-1 is not

17 sphorylated ERK1/ERK2 expression following a hypotonic shock was up-regulated by protein kinase C (PK

18 ury resulting from DNA alkylating agents and hypotonic shock, whereas it promotes a caspase-8-mediate

19  in contrast to volume regulation induced by hypotonic shock, which appears to require extracellular