Evidence map›Paper›PMID 17486064›Full record

ArticleOncogene2007

Human p16gamma, a novel transcriptional variant of p16(INK4A), coexpresses with p16(INK4A) in cancer cells and inhibits cell-cycle progression.

Y-C Lin, M B Diccianni, Y Kim, H-H Lin, C-H Lee, R-J Lin, S H Joo, J Li, T-J Chuang, A-S Yang and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

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  9. Deep exploration of aJournal of medical genetics · 2022
    Article
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  12. Precision medicine in Ewing sarcoma: a translational point of view.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Review
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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

13 authors at 3 institutions in 2 countries.

Y-C LinGenomics Research Center, Academia Sinica, Taipei, Taiwan.
M B Diccianni
Y Kim
H-H Lin
C-H Lee
R-J Lin
S H Joo
J Li
T-J Chuang
A-S Yang
H-H Kuo
M-D Tsai
A L Yu
Genomics Research Center, Academia Sinica · TWUniversity of California, San Diego · USThe Ohio State University · US

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
STRUCTURE FUNCTION RELATIONSHIP OF TUMOR SUPRESSORSR01CA069472 · NCI · OHIO STATE UNIVERSITY · PI LI, JUNAN · 1996 to 2009
$2.4M
NCI NIH HHS 2 P30CA23100-18NCI NIH HHS CA69472
6 · The paper itself

Abstract

The INK4A locus encodes two tumor suppressor genes, p16(INK4A) and p14(ARF), transcribed using alternative exons 1alpha or 1beta spliced onto the same exons 2 and 3. Both p16(INK4A) and p14(ARF) are capable of inhibiting the cell-cycle progression, albeit in different manner; p16(INK4A) is phosphorylation of retinoblastoma (pRB) dependent while p14(ARF) is p53-dependent. In this study, we report the discovery of a novel variant of p16(INK4A), termed p16gamma, in a primary T-cell acute lymphoblastic leukemia (T-ALL) patient sample and a neuroblastoma cell line, which was expressed at both the transcriptional and translational levels. Cloning and sequencing of the p16gamma cDNA revealed that p16gamma was identical to p16(INK4A), except that it contained an in-frame insertion of 197 bp between exons 2 and 3. p16gamma expression was detected in the majority of p16(INK4A)-expressing primary T-ALL and B-ALL patient samples and other p16(INK4A)-expressing tumor samples, but was only barely detectable in some normal mononuclear cells and other non-tumor samples. Structural analysis by nuclear magnetic resonance and circular dichroism confirmed that p16gamma, like p16(INK4A), is also an ankyrin-repeat protein. Functional analysis of p16gamma revealed that p16gamma protein interacted with cyclin D-dependent kinase4 and inhibited its kinase activity. Using a luciferase reporter assay, the transfection of p16gamma repressed the E2F response, the downstream target of pRB, with an efficacy equivalent to that of p16(INK4A). Moreover p16gamma, like p16(INK4A), induced cell-cycle arrest at G(0)/G(1), and inhibited cell growth in colony formation assay.

Indexed as

G1 PhaseResting Phase, Cell CycleAlternative SplicingBlotting, WesternBurkitt LymphomaCircular DichroismColony-Forming Units AssayCyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p16E2F Transcription FactorsHumansImmunoprecipitationLeukemia-Lymphoma, Adult T-CellLuciferasesNeuroblastomaTwo-Hybrid System TechniquesCyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p16E2F Transcription FactorsLuciferases

Identifiers

PMID17486064
OpenAlexW2104354950

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.