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After Toohey found that some murine leukemia cell lines lack MTAP [3], others reported that many of the most common human tumors are also deficient in MTAP.
Being N2a-PK1 cellsusceptiblele to only some murine prion strains, these cells cannot evaluate contamination by scrapie and CWD prions, the most relevant for environmental infectivity.
Down regulation of the kinesin motor protein Kif1C resulted in the resistance of some murine macrophages to LeTx induced cytotoxicity, whereas up-regulation of this protein increased the sensitivity of cells to LeTx [15].
Antibodies which block CTLA-4 or which activate 4-1BB can promote the rejection of some murine tumors, but fail to cure poorly immunogenic tumors like B16 melanoma as single agents.
Prior studies have shown that agonistic 4-1BB antibodies with or without CTLA-4 blockade can promote the rejection of some murine tumors and ameliorate auto-immune toxicity; however, poorly immunogenic tumors such as B16 melanoma do not respond to antibody therapy alone [10], [14].
The present in vitro results suggest that the anti-inflammatory effects of PAR1 deficiency, already described in some murine models, may relate in part to the absence of pro-survival signaling mediated by certain agonists such as KLK6 at this receptor, and therefore increased vulnerability of lymphocytes to apoptosis.
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Complications related to allergic reactions were noted for some murine-based proteins.
In some instances, murine models of allergic asthma have not recapitulated the human findings, and have led to some costly failures in drug development.
The speckled distribution of Aβ immunoreactivity within the neuronal perikarya closely resembles the intracellular Aβ immunoreactive pattern documented for human AD as well as some other murine AD models, where it is detectable in vulnerable brain regions preceding plaque deposition and the development of neurofibrillary changes [19], [20].
Many reports have shown that some of murine anti-PrP mAbs that did not distinguish between PrPC and PrPSc were nevertheless able to prevent prion infection in vitro [19], [20], [21], [22], and a few studies also demonstrated in vivo anti-prion action of such mAbs [9], [23], [24].
This analysis shows strong evidence in support of accelerated evolution in some Ang murine copies (mAng).
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