IGFBP6 Modulates Proteostasis by Activating ATF4 Targets and Reducing ER Retrotranslocon Expression.

O E Kolodeeva, O E Kolodeeva, I D Antipenko, A A Fatkulin, M R Yakhina, J A Makarova

Abstract read

In one paragraph

Article in Doklady. Biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

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

1 citing paper in PubMed.

The Impact of IGFBP6 Knockdown on Cholesterol Metabolism in Breast Cancer Cells.Current medicinal chemistry · 2026
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

6 authors.

O E KolodeevaFaculty of Biology and Biotechnology, National Research University Higher School of Economics, Moscow, Russia.

I D AntipenkoFaculty of Biology and Biotechnology, National Research University Higher School of Economics, Moscow, Russia.

A A FatkulinFaculty of Biology and Biotechnology, National Research University Higher School of Economics, Moscow, Russia.

M R YakhinaFaculty of Biology and Biotechnology, National Research University Higher School of Economics, Moscow, Russia.

J A MakarovaFaculty of Biology and Biotechnology, National Research University Higher School of Economics, Moscow, Russia. jmakarova@hse.ru.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reduced expression of the IGFBP6 protein leads to an increase in the metastatic potential of breast cancer (BC) cells. The level of protein synthesis in tumor cells is increased, leading to a compensatory adjustment of proteostasis. One of the tools used to study proteostasis is protein toxins of the RIP-II family, which irreversibly inactivate ribosomes (particularly, viscumin). We investigated the effect of IGFBP6 gene knockdown on the proteostasis in the BC cell line MDA-MB-231. Ribosomes from MDA-MB-231

Indexed as

Activating Transcription Factor 4Endoplasmic ReticulumEndoplasmic Reticulum-Associated DegradationInsulin-Like Growth Factor Binding Protein 6ProteostasisBreast NeoplasmsCell Line, TumorFemaleHumansRibosomesUnfolded Protein ResponseActivating Transcription Factor 4ATF4 protein, humanInsulin-Like Growth Factor Binding Protein 6ERERADIGFBP6MDA-MB-231UPRviscumin

Identifiers

PMID39480639

DOI10.1134/S1607672924600714

PMCPMC11739220

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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.