Evidence map›Paper›PMID 37122440›Full record

ArticleAdvanced theory and simulations2023

Rational Design of de novo CCL2 Binding Peptides.

Erika Davidoff Aguas, Abdul-Rahman Azizogli, Jatin Kashyap, Joseph Dodd-O, Zain Siddiqui, Jay Sy, Vivek Kumar

Open access · greenAbstract read
In one paragraph

Article in Advanced theory and simulations, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
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

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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

7 authors at 2 institutions in 1 country.

Erika Davidoff AguasDepartment of Biomedical Engineering, Rutgers University, Piscataway, NJ, 08544.
Abdul-Rahman AzizogliDepartment of Biological Sciences, New Jersey Institute of Technology, Newark, NJ, 07102.
Jatin KashyapDepartment of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ, 07102.
Joseph Dodd-ODepartment of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ, 07102.
Zain SiddiquiDepartment of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ, 07102.
Jay SyDepartment of Biomedical Engineering, Rutgers University, Piscataway, NJ, 08544.
Vivek KumarDepartment of Biological Sciences, New Jersey Institute of Technology, Newark, NJ, 07102.
New Jersey Institute of Technology · USRutgers, The State University of New Jersey · US

Funding

X-RAY STRUCTURE OF RIFM PROTEIN FROM THE BIOSYNTHESIS PATHWAY OF THE ANSAMYCIN AP41RR012408 · NCRR · BROOKHAVEN SCIENCE ASSOC-BROOKHAVEN LAB · PI ORVILLE, ALLEN M · 1998 to 2011
$32.2M
New Jersey Alliance for Clinical Translational Science: NJ ACTSUL1TR003017 · NCATS · RUTGERS BIOMEDICAL/HEALTH SCIENCES-RBHS · PI PANETTIERI, REYNOLD ALEXANDER · 2019 to 2023
$28.9M
Rutgers Biotechnology Training ProgramT32GM135141 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI ANN M. STOCK, Martin L Yarmush · 2020 to 2026
$3.5M
Bioactive Scaffold for TMJ Disc Regeneration by Endogenous Stem/Progenitor CellsR01DE029321 · NIDCR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LEE, CHANG HUN · 2020 to 2024
$3.5M
Diversity Supplement for Angiogenic and anti-microbial supports for pulp regenerationR01DE031812 · NIDCR · UNIVERSITY OF HOUSTON · PI Vivek Kumar · 2022 to 2026
$3.3M
Peptide hydrogels for management and treatment of neovascular posterior segment diseasesR15EY029504 · NEI · NEW JERSEY INSTITUTE OF TECHNOLOGY · PI KUMAR, VIVEK · 2019 to 2020
$508k
Acellular composite hydrogel scaffolds for volumetric muscle regenerationR21AR079708 · NIAMS · NEW JERSEY INSTITUTE OF TECHNOLOGY · PI GRASMAN, JONATHAN M., KUMAR, VIVEK · 2022 to 2023
$467k
NCATS NIH HHS UL1 TR003017NCRR NIH HHS P41 RR012408NEI NIH HHS R15 EY029504NIAMS NIH HHS R21 AR079708NIDCR NIH HHS R01 DE029321NIDCR NIH HHS R01 DE031812NIGMS NIH HHS T32 GM135141
6 · The paper itself

Abstract

Chronic levels of inflammation lead to autoimmune diseases such as rheumatoid arthritis and atherosclerosis. A key molecular mediator responsible for the progression of these diseases is Chemokine C-C motif ligand 2 (CCL2), a homodimerized cytokine that dissociates into monomeric form and binds to the CCR2 receptor. CCL2, also known as monocyte chemoattractant protein-1 (MCP-1), attracts monocytes to migrate to areas of injury and mature into macrophages, leading to positive feedback inflammation with further release of proinflammatory molecules such as IL-1β and TNF-α. Sequestering CCL2 to prevent its binding to CCR2 may prevent this inflammatory activity. Prior work adapted an α-helical CCL2-binding peptide (WKNFQTI) from murine CCR2 through extracellular loop analysis. Here, higher-affinity peptide binders were computationally designed through homology modeling and energy calculations, yielding an 11-amino acid peptide with high binding affinity. In addition, Rosetta mutations improved binding affinity

Indexed as

CCR2computational peptide designinflammationMCP-1molecular docking

Identifiers

PMID37122440
PMCPMC10139756
OpenAlexW4311869294

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.