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So far, no mouse models deficient in Fam162a, Ccdc58, Csta, or Stfa2l1 have been described.
Recently, the function of AAMs was addressed either by depleting them or by using mouse models deficient in their signature molecules like Arg1 and Fizz1.
We have designed this approach to create cellular models deficient in vitamin B12 (cobalamin) because of the known problematics associated to the obtainment of effective vitamin B12 deficient cell models.
The thymopoietic phenotypes of Cdc42−/− mice are reminiscent of and complementary to the previous observations in mouse models deficient in Rac1, Rac2 or RhoH, other members of Rho family GTPases.
Animal models deficient in seipin recapitulate the human lipodystrophic phenotype.
This is in line with embryonic lethality due to myocardial rupture in mice models deficient in these proteins.
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We chose the Rag1-/ mouse model deficient in both mature T and B lymphocytes [23].
We present the first evidence from a mouse model deficient in ankyrin-B that ankyrin-B variants can be viewed as balanced variants with increased risk of sudden death and early aging offset by increased cardiac contractility.
Overall, this study presents an optimized approach to globally monitor cystatin gene expression as well as a new mouse model deficient in Stfa2l1/Csta genes, expanding the available tools to dissect cystatin roles under normal and pathological conditions.
To cause deprivation of vitamin B12, we have recently developed a cell model deficient in B12 by anchoring transcobalamin (TCII) to the endoplasmic reticulum through its fusion with Oleosin (OLEO), a plant protein localized to lipid droplets and endoplasmic reticulum of plant cells [16] [18].
Here, we describe a novel mouse model deficient in SAFB2.
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Justyna Jupowicz-Kozak
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