Evidence map›Paper›PMID 39227740›Full record

ArticleCommunications chemistry2024

Mechanism of activation and autophosphorylation of a histidine kinase.

Mayukh Kansari, Fathia Idiris, Hendrik Szurmant, Tomáš Kubař, Alexander Schug

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In one paragraph

Article in Communications chemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Mayukh Kansari *Institute of Physical Chemistry, Karlsruhe Institute of Technology, Karlsruhe, Germany.
Fathia Idiris *Steinbuch Centre for Computing, Karlsruhe Institute of Technology, Karlsruhe, Germany.
Hendrik SzurmantCollege of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA, USA.ORCID http://orcid.org/0000-0002-6970-9566
Tomáš KubařInstitute of Physical Chemistry, Karlsruhe Institute of Technology, Karlsruhe, Germany.ORCID http://orcid.org/0000-0002-2419-6912
Alexander SchugJülich Supercomputing Centre, Forschungszentrum Jülich, Jülich, Germany. al.schug@fz-juelich.de.ORCID http://orcid.org/0000-0002-0534-502X

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) INST 40/575-1 FUGGHelmholtz Association NIC
6 · The paper itself

Abstract

Histidine kinases (HK) are one of the main prokaryotic signaling systems. Two structurally conserved catalytic domains inside the HK enable autokinase, phosphotransfer, and phosphatase activities. Here, we focus on a detailed mechanistic understanding of the functional cycle of the WalK HK by a multi-scale simulation approach, consisting of classical as well as hybrid QM/MM molecular dynamics simulation. Strikingly, a conformational transition induced solely in DHp leads to the correct activated conformation in CA crucial for autophosphorylation. This finding explains how variable sensor domains induce the transition from inactive to active state. The subsequent autophosphorylation inside DHp proceeds via a penta-coordinated transition state to a protonated phosphohistidine intermediate. This intermediate is consequently deprotonated by a suitable nearby base. The reaction energetics are controlled by the final proton acceptor and presence of a magnesium cation. The slow rates of the process result from the high energy barrier of the conformational transition between inactive and active states. The phosphorylation step exhibits a lower barrier and down-the-hill energetics. Thus, our work suggests a detailed mechanistic model for HK autophosphorylation.

Identifiers

PMID39227740
PMCPMC11371814

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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.