Loss of Slfn3 induces a sex-dependent repair vulnerability after 50% bowel resection | Zendy

Emilie E. VomhofDeKrey | Zendy; Jack Lansing | Zendy; Diane C. Darland | Zendy; Josey Umthun | Zendy; Allie D. Stover | Zendy; Christopher C. Brown | Zendy; Marc D. Basson | Zendy

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Loss of Slfn3 induces a sex-dependent repair vulnerability after 50% bowel resection

Author(s) -

Emilie E. VomhofDeKrey,

Jack Lansing,

Diane C. Darland,

Josey Umthun,

Allie D. Stover,

Christopher C. Brown,

Marc D. Basson

Publication year - 2020

Publication title -

ajp gastrointestinal and liver physiology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.644

H-Index - 169

eISSN - 1522-1547

pISSN - 0193-1857

DOI - 10.1152/ajpgi.00344.2020

Subject(s) - biology , crypt , enterocyte , cell growth , conditional gene knockout , downregulation and upregulation , cellular differentiation , immunology , microbiology and biotechnology , endocrinology , medicine , cancer research , andrology , small intestine , phenotype , gene , genetics

The differentiating stimulus of Slfn3 signaling restrains an increase in mucosal mass after bowel resection, and there is a Slfn3-sex interaction regulating differentiation gene expression and intestinal adaptation. This current study highlights the combinatory effects of gender and Slfn3 genotype on the gene expression changes that contribute to the adaptation in intestinal cellular milleu (i.e. villus and crypt structure) which are utilized to compensate for the stress-healing response that the animals display in intestinal adaptation.

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