ArticleMolecular reproduction and development2021
Generation and analysis of Prss28 and Prss29 deficient mice using CRISPR-Cas9 genome-editing.
Article in Molecular reproduction and development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Progesterone receptor in uterine glands is required for pregnancy establishment in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Hallmarks of uterine receptivity predate placental mammals.bioRxiv : the preprint server for biology · 2024Article
- Attenuated retinoic acid signaling is among the early responses in mouse uterus approaching embryo attachment.Reproductive and developmental medicine · 2024Article
- Activation function 1 of progesterone receptor is required for progesterone antagonism of oestrogen action in the uterus.BMC biology · 2022Article
- Spatial transcriptomic profiles of mouse uterine microenvironments at pregnancy day 7.5†.Biology of reproduction · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Glands of the uterus are essential for the establishment of pregnancy in mice and their products regulate embryo implantation and stromal cell decidualization critical for pregnancy establishment. Forkhead box A2 (FOXA2) is expressed specifically in the glands and a critical regulator of their differentiation, development and function. Progesterone and FOXA2 regulate members of a serine proteinase gene family (Prss28 and Prss29). Here, CRISPR-Cas9 genome-editing was used to create mice with a heterozygous or homozygous deletion of Prss28 or/and Prss29 to determine their biological roles in uterine function. Female mice lacking Prss28 and Prss29 or both developed normally and were fertile without alterations in uterine histoarchitecture, uterine gland number, or and gene expression. Thus, Prss28 and Prss29 are dispensable for female fertility and do not impact endometrial gland development or uterine function mice.
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