ArticleThe journal of physical chemistry. B2018
Interface Residues That Drive Allosteric Transitions Also Control the Assembly of l-Lactate Dehydrogenase.
Article in The journal of physical chemistry. B, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed, 11 citations in OpenAlex.
- Allosteric regulation of L-lactate dehydrogenase: Beyond effector-mediated tetramerization.Protein science : a publication of the Protein Society · 2025Article
- Cooperativity and Folding Kinetics in a Multidomain Protein with Interwoven Chain Topology.ACS central science · 2022Article
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 at 2 institutions in 1 country.
Funding
Abstract
The allosteric enzyme, l-lactate dehydrogenase (LDH), is activated by fructose 1,6-metaphosphate (FBP) to reduce pyruvate to lactate. The molecular details of the FBP-driven transition from the low affinity T state to the high affinity R state in LDH, a tetramer composed of identical subunits, are not known. The dynamics of the T → R allosteric transition, investigated using Brownian dynamics (BD) simulations of the self-organized polymer (SOP) model, revealed that coordinated rotations of the subunits drive the T → R transition. We used the structural perturbation method (SPM), which requires only the static structure, to identify the allostery wiring diagram (AWD), a network of residues that transmits signals across the tetramer, as LDH undergoes the T → R transition. Interestingly, the residues that play a major role in the dynamics, which are predominantly localized at the interfaces, coincide with the AWD identified using the SPM. Although the allosteric pathways are highly heterogeneous, on the basis of our simulations, we surmise that predominantly the conformational changes in the T → R transition start from the region near the active site, comprised of helix αC, helix α1/2G, helix α3G, and helix α2F, and proceed to other structural units, thus completing the global motion. Brownian dynamics simulations of the tetramer assembly, triggered by a temperature quench from the fully disrupted conformations, show that the bottleneck for assembly is the formation of the correct orientational registry between the subunits, requiring contacts between the interface residues. Surprisingly, these residues are part of the AWD, which was identified using the SPM. Taken together, our results show that LDH, and perhaps other multidomain proteins, may have evolved to stabilize distinct states of allosteric enzymes using precisely the same AWD that also controls the functionally relevant allosteric transitions.
Indexed as
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.