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While gene variants of FGFR2 may influence the risk of hypospadias in humans [26], conditional inactivation of FGFR2 in mouse models resulted in blockade of the XY-specific gonad growth and disruption of testis differentiation, leading to a male-to-female sex reversal phenotype.
Immunotherapy targeting amyloid deposition in both mouse models resulted in decreased alternative inflammatory markers and, in the case of passive immunization, a transient increase in pro-inflammatory markers.
Interestingly, globally decreasing Fli1 levels by 50% in two different lupus mouse models resulted in significantly improved disease, most notably improved nephritis, accompanied by significantly prolonged survival [ 4, 6].
Germline ablation of Lrig1 in two independent mouse models resulted in elevated levels of ErbB1-3 in the intestine (Powell et al, 2012; Wong et al, 2012), providing in vivo evidence to support its role in degrading ErbBs.
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Different mouse models resulting in either a null allele or Mecp2 truncating mutations recapitulate RTT-like phenotypes (14– 14).
The take-home lesson here is that the majority of these mouse models result in tumors that resemble human breast adenocarcinomas pathologically.
Dramatic effects of PGRN deficiency have been shown in vivo in collagen-induced arthritis and collagen Ab-induced arthritis mouse models, resulting in fulminant courses of disease [ 14].
Most genetically engineered mouse models result in rapidly developing tumours with one single genotype in mice that are also genetically homogeneous: such models test the interaction of a single cancer genome with a single host genome.
More recently, it was reported that BMP signaling can inhibit Wnt activity, which functionally designates the colon CSCs, in mouse models resulting in suppressed crypt formation and reduced polyp growth [ 25].
Further studying the role of ATP6AP2 in transcription regulation and, specifically, to what extent the synaptic and behavioural phenotypes observed in Drosophila and mouse models result from abnormal Wnt and/or MAP kinases ERK1/2 signalling will be extremely interesting.
Search terms encompassed all aspects of spermatogenesis, post-testicular sperm maturation and knockout mouse models resulting in male infertility, including, but not limited to, spermatogenesis, testis, sperm, spermatozoa and epididymis.
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