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In particular, pre-clinical models resembling human pathologies are necessary.
Using our established cell and knockout/transgenic mouse models resembling human NS harboring the R246Q or C321R mutation respectively, we have shown that both R246Q and C321R mutations cause defective secretion of laminin-521 from podocytes to the GBM [ 49, 50].
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These models resemble human breast cancer with respect to progression and metastasis [ 29, 30].
We and others have recently reported that in vitro organotypic human-derived tracheal/bronchial epithelium pseudostratified models resemble human respiratory tract epithelium at the morphological and molecular levels [ 30– 30].
Some of these models resemble human HCCs and have contributed to varying degrees towards understanding the mechanisms and genes involved in HCC formation, highlighting the relevance of such mouse models.
Until a model resembling human OSCC is developed, both the advantages and disadvantages of each model should be carefully considered.
Collectively, our data suggest that the PlnOE mouse is a novel myopathy model resembling human centronuclear myopathy (CNM), with additional dystrophic features and potential core-like lesions.
MS, for a long time, was considered as a Th1-dependent disease, until studies revealed the key role of Th17 cells and IL-17 family cytokines in the development of MS using EAE, a mouse model resembling human MS. Th17 cells and associated cytokines are the major force that drives the related central nervous system inflammation and lesion formation.
Mouse atherosclerosis models resemble humans in that the most prominent cells involved in lesion development are monocyte-derived macrophages and T-lymphocytes.
Over the years, swine have been one of the most frequently used model resembling humans in almost all aspects analyzed.
A "knock-in" mouse model resembles human TBS more closely, indicating that domain-negative effort is responsible for the pathogenesis of TBS.
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