First-pass extracted concept

CRY2 S510L

Candidate: toolkit item1 source documents5 linked claims

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Aliases

mouse CRY2 S510L

Evidence Snippets

two orthologous mutations of mouse CRY2 (D325H and S510L)

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1primary paper2021Proceedings of the National Academy of SciencesDOI PubMed

1 evidence snippet 5 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1expression effectsupports2021Source 1DOI PubMed

CRY2 D325H and CRY2 S510L do not affect steady-state levels of overexpressed c-MYC.

Quoted textsource-backed

Neither mutant affects steady-state levels of overexpressed c-MYC

Claim 2functional effectsupports2021Source 1DOI PubMed

CRY2 D325H and CRY2 S510L accelerate the growth of primary mouse fibroblasts expressing high levels of c-MYC.

Quoted textsource-backed

We demonstrate that two orthologous mutations of mouse CRY2 (D325H and S510L) accelerate the growth of primary mouse fibroblasts expressing high levels of c-MYC.

Claim 3gene expression effectsupports2021Source 1DOI PubMed

Stable expression of CRY2 D325H or CRY2 S510L robustly suppresses P53 target-gene expression.

Quoted textsource-backed

stable expression of either CRY2 D325H or of CRY2 S510L robustly suppresses P53 target-gene expression

Claim 4mechanistic effectmixed2021Source 1DOI PubMed

CRY2 D325H and CRY2 S510L have divergent impacts on circadian rhythms and on the ability of CRY2 to interact with SCF FBXL3.

Quoted textsource-backed

they have divergent impacts on circadian rhythms and on the ability of CRY2 to interact with SCF<sup>FBXL3</sup>

Claim 5mechanistic hypothesissupports2021Source 1DOI PubMed

Suppression of P53 target-gene expression may be a primary mechanism by which CRY2 D325H and CRY2 S510L influence cell growth.

Quoted textsource-backed

suggesting that this may be a primary mechanism by which they influence cell growth