ArticleNature communications2026
Enabling molecular signaling with temperature and ionic-strength independence or programmable dependence.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The equilibrium constants of chemical reactions fundamentally depend on temperature, posing challenges for living systems. However, many conformer organisms do not maintain a stable internal temperature. This raises the question: can molecular signaling pathways inherently resist temperature susceptibility? Molecular commutation is a recently discovered, fundamentally distinct mechanism of biological information processing and storage within reversible association/dissociation reactions. Here, we show that molecular commutation enables complex signaling systems that are independent of temperature and ionic strength and, even more generally, programmably dependent on these parameters. Using examples of various DNA logic gates, receptor-activator networks, and systems with complex input-output relationships (e.g., computed as algebraic functions), we demonstrate computationally that introducing compensatory reactions in these networks can render their signaling independent of temperature and ionic strength. We experimentally validate such independence for a case of a YES-logic gate. Finally, we computationally demonstrate networks with outputs that follow predefined functional forms of temperature and ionic strength (e.g., sin(T), where T is temperature). The presented intrinsic capabilities of affinity-based networks provide a remarkable homeostasis and signaling control mechanism that may be used by biological systems of arbitrarily high complexity.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.