Evidence map›Paper›PMID 31408950›Full record

ArticleMaterials (Basel, Switzerland)2019

Activating the Intrinsic Pathway of Apoptosis Using BIM BH3 Peptides Delivered by Peptide Amphiphiles with Endosomal Release.

Mathew R Schnorenberg, Joseph A Bellairs, Ravand Samaeekia, Handan Acar, Matthew V Tirrell, James L LaBelle

Open access · goldAbstract read
In one paragraph

Article in Materials (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Inhibition of FOXP3 by stapled alpha-helical peptides dampens regulatory T cell function.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021
    Review
  9. Review
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

6 authors at 1 institution in 1 country.

Mathew R SchnorenbergPritzker School of Molecular Engineering, University of Chicago, Chicago, IL 60637, USA.ORCID 0000-0002-2876-573X
Joseph A BellairsDepartment of Pediatrics, Section of Hematology/Oncology, University of Chicago, Chicago, IL 60637, USA.
Ravand SamaeekiaPritzker School of Molecular Engineering, University of Chicago, Chicago, IL 60637, USA.ORCID 0000-0003-4237-1291
Handan AcarPritzker School of Molecular Engineering, University of Chicago, Chicago, IL 60637, USA.
Matthew V TirrellPritzker School of Molecular Engineering, University of Chicago, Chicago, IL 60637, USA.
James L LaBelleDepartment of Pediatrics, Section of Hematology/Oncology, University of Chicago, Chicago, IL 60637, USA. jlabelle@peds.bsd.uchicago.edu.ORCID 0000-0001-6776-4695
University of Chicago · US

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI MARK W. LINGEN · 1985 to 2026
$122.1M
A Potent and Specific Approach to Targeting B-Cell Lymphoma: Disrupting Malignant Protein-Protein Interactions Using CD19-Targeted Stapled Peptide Amphiphile NanoparticlesF30CA221250 · NCI · UNIVERSITY OF CHICAGO · PI SCHNORENBERG, MATHEW RYAN · 2017 to 2021
$250k
Hoogland Lymphoma Research Award NANCI NIH HHS F30 CA221250NCI NIH HHS P30 CA014599NIH F30 F30CA221250University of Chicago MSTP Training Grant T32GM007281
6 · The paper itself

Abstract

Therapeutic manipulation of the BCL-2 family using BH3 mimetics is an emerging paradigm in cancer treatment and immune modulation. For example, peptides mimicking the BIM BH3 helix can directly target the full complement of anti- and pro-apoptotic BCL-2 proteins to trigger apoptosis. This study has incorporated the potent BH3 α-helical death domain of BIM into peptide amphiphile (PA) nanostructures designed to facilitate cellular uptake and induce cell death. This study shows that these PA nanostructures are quickly incorporated into cells, are able to specifically bind BCL-2 proteins, are stable at physiologic temperatures and pH, and induce dose-dependent apoptosis in cells. The incorporation of a cathepsin B cleavable linker between the BIM BH3 peptide and the hydrophobic tail resulted in increased intracellular accumulation and mitochondrial co-localization of the BIM BH3 peptide while also improving BCL-2 family member binding and apoptotic reactivation. This PA platform represents a promising new strategy for intracellular therapeutic peptide delivery for the disruption of intracellular protein:protein interactions.

Indexed as

apoptosisBCL-2 familyBH3-onlyBIMcathepsinpeptide amphiphilepeptide therapeutics

Identifiers

PMID31408950
PMCPMC6719084
OpenAlexW2969069368

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.