Evidence map›Paper›PMID 27590344›Full record

ArticleThe Journal of biological chemistry2016

Death-associated Protein Kinase-1 Expression and Autophagy in Chronic Lymphocytic Leukemia Are Dependent on Activating Transcription Factor-6 and CCAAT/Enhancer-binding Protein-β.

Padmaja Gade, Amy S Kimball, Angela C DiNardo, Priyamvada Gangwal, Douglas D Ross, H Scott Boswell, Susan K Keay, Dhananjaya V Kalvakolanu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Cell surface GRP78 and the UPR pathway as novel promising therapeutic targets in cancer: an insight into the treatment of acute leukemia by using GRP78-CART cells.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Autophagy and Metabolism in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2021
    Review
  9. Review
  10. Review
  11. The Ontogeny of a Neutrophil: Mechanisms of Granulopoiesis and Homeostasis.Microbiology and molecular biology reviews : MMBR · 2018
    Review
  12. Article
  13. 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

8 authors at 1 institution in 1 country.

Padmaja GadeFrom the Departments of Microbiology and Immunology and.
Amy S KimballMedicine and.
Angela C DiNardoFrom the Departments of Microbiology and Immunology and.
Priyamvada GangwalFrom the Departments of Microbiology and Immunology and.
Douglas D RossMedicine and the Greenebaum Comprehensive Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201, the Baltimore Veterans Affairs Medical Center, Baltimore, Maryland 21201, and.
H Scott Boswellthe Indianapolis Veterans Affairs Medical Center, Indianapolis, Indiana 46202.
Susan K KeayMedicine and the Baltimore Veterans Affairs Medical Center, Baltimore, Maryland 21201, and.
Dhananjaya V KalvakolanuFrom the Departments of Microbiology and Immunology and dkalvako@umaryland.edu.
U-M Rogel Cancer Center

Funding

MODULATION OF IFN ACTION VIA NOVEL REGULATORY FACTORSR01CA078282 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI KALVAKOLANU, DHAN V. · 1998 to 2014
$4.4M
NCI NIH HHS R01 CA078282
6 · The paper itself

Abstract

Expression of DAPK1, a critical regulator of autophagy and apoptosis, is lost in a wide variety of tumors, although the mechanisms are unclear. A transcription factor complex consisting of ATF6 (an endoplasmic reticulum-resident factor) and C/EBP-β is required for the IFN-γ-induced expression of DAPK1 IFN-γ-induced proteolytic processing of ATF6 and phosphorylation of C/EBP-β are obligatory for the formation of this transcriptional complex. We report that defects in this pathway fail to control growth of chronic lymphocytic leukemia (CLL). Consistent with these observations, IFN-γ and chemotherapeutics failed to activate autophagy in CLL patient samples lacking ATF6 and/or C/EBP-β. Together, these results identify a molecular basis for the loss of DAPK1 expression in CLL.

Indexed as

AutophagyGene Expression Regulation, EnzymologicGene Expression Regulation, LeukemicActivating Transcription Factor 6CCAAT-Enhancer-Binding Protein-betaCell Line, TransformedDeath-Associated Protein KinasesFemaleHumansInterferon-gammaLeukemia, Lymphocytic, Chronic, B-CellMaleNeoplasm ProteinsActivating Transcription Factor 6ATF6 protein, humanCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanDAPK1 protein, humanDeath-Associated Protein KinasesIFNG protein, humanInterferon-gammaNeoplasm Proteinscell signalingcytokine actionendoplasmic reticulum stress (ER stress)transcription factortumor suppressor gene

Identifiers

PMID27590344
PMCPMC5063986
OpenAlexW2513388740

What OpenQuestion holds

Textmetadata
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.