The Claim
High expression levels of GPR35 cause strong constitutive activation of Gα12 and Gα13, which prevents the detection of additional signaling effects from agonists, while low expression levels of GPR35 permit the observation of agonist-induced signaling responses.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
When GPR35 is present in high amounts, it continuously activates Gα12 and Gα13 proteins, making it impossible to detect signals triggered by other molecules. When GPR35 is present in low amounts, signals from those other molecules can be detected.
See the scientific wording
High expression levels of GPR35 lead to strong constitutive activation of Gα12 and Gα13, which masks the ability to detect additional signaling effects from agonists, whereas low expression allows agonist-induced responses to be observed.
When there are many GPR35 receptors on a cell, they are always active on their own and strongly turn on Gα12 and Gα13 proteins, so adding a drug that should activate them makes no extra difference. When there are few receptors, the drug can clearly turn them on and activate Gα12 and Gα13, because there is no background noise from constant activity.
What the research says
1 studyWhen there are lots of GPR35 receptors, they’re already super active on their own, so adding a drug doesn’t make things any more active — it’s like turning up a stereo that’s already at max volume. But when there are few receptors, the drug can clearly make them more active.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.