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A few key studies have examined the importance of SIRT1 within the β-cell and demonstrated that SIRT1 overexpression or knock-out mouse models display increased or decreased insulin secretion respectively1,2.
Second, the transgenic mouse models display aberrant expression of peptide-specific TCRα and β transgenes, which bypasses the thymic negative selection and consequently lead to the escape of an unusual large number of autoreactive T-cells in periphery [38].
Whereas, in humans, CL/P is more common than CP, most mouse models display CP.
Previous Notch-driven mammary-tumor mouse models display varying phenotypes, ranging from mammary hyperplasia and DCIS in nulliparous mice to lactation-dependent regressing tumors and nonregressing invasive adenocarinomas [ 8, 31- 33].
Some of these mouse models display embryonic lethality, others relatively little phenotype, but several have clinical phenotypes similar to the respective human diseases, enabling preclinical trials to be performed.
For the Wnts, none of the published Wnt knockout mouse models display a phenotype that would suggest a clear role in patterning of the nephron, although both Wnt9b and Wnt7b, when deleted, alter nephron morphogenesis.
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In particular, AD transgenic mouse models displayed a strikingly reduced Aβ burden in the hippocampus and cortex when SIRT1 was chemical activated or overexpressed by lentiviral infection (Karuppagounder et al., 2009).
Notably, these conditional mouse models displayed most of the distinctive neurological features of TSC.
Regarding cancer initiation, knockout mouse models displaying constitutive autophagic inhibition appear to be useful.
Similarly, AHR is a common feature of mouse models displaying an obese phenotype, such as ob/ ob mice that lack the satiety hormone leptin, db/ db mice that lack the leptin receptor, or Cpe fat mice that lack carboxypeptidase E, which is involved in the processing of neuropeptides that mediate eating disorders (Shore, 2010).
To further compare the phenotype of podoplanin+ CD31− stromal cells found in TLTs with their counterparts in LNs, a panel of markers was tested on pancreatic infiltrates of RIP-CXCL13 transgenic RIP-CXCL13 transgenice three micee models, displayed the highest frequency of large infiltrates and lymphoid tissue structures.
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