Demo corpus. Scores are computed on a select set of biomedical paper/datasets and may be inaccurate for papers outside this corpus — DataRank relies on network effects that improve with scale. We aim to expand this into a fully open resource pending additional funding.

Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor

Cell(1999)10.1016/s0092-8674(00)80595-4Source: DataRank Database

Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor is a research paper published in Cell (1999). On theSindex it has a DataRank of 1.3. It has been cited 6,545 times.

N/A

1.3DataRank · unranked

1.3

Open Access6545 citations · base score 8.8

Cite:

datarank_citation_only_1hop_v6· scope data_onlyMethodology

Abstract

Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/ threonine kinase Akt, which then phosphorylates and inactivates components of the apoptotic machinery, including BAD and Caspase 9. In this study, we demonstrate that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors. In the presence of survival factors, Akt phosphorylates FKHRL1, leading to FKHRL1's association with 14-3-3 proteins and FKHRL1's retention in the cytoplasm. Survival factor withdrawal leads to FKHRL1 dephosphorylation, nuclear translocation, and target gene activation. Within the nucleus, FKHRL1 triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.

›Data sources & pipeline

Pipeline:MetadataData-paper checkEnrichmentCitation networkScoring

Enrichment:Pending

FAIR Checklist

Context only (not used in score)

Findable (1/2)

Has DOI

Accessible (1/2)

Open Access

Interoperable (0/2)

Reusable (0/3)

FAIR checklist signals are shown for context only and do not affect DataRank scoring.

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DataRank Breakdown

Base Score 100%Citation Network 0%

Base Score Contribution

1.3

From this paper's citation signal

Citation Network Contribution

Citation network not refreshed for this result

This paper's DataRank is currently driven only by its base citation score. Citation network data was not refreshed for this result.

Learn more about DataRank methodology →

Why this DataRank?

DataRank blends this paper's own citation count with the influence of the papers that cite it. Here, roughly 100% comes from its base citations and 0% from the citation network.

Base score B(p): log1p(citation_count) — grows sub-linearly, so a paper with 1,000 citations is not 10× a paper with 100.
Network N(p): Σ over citers of log1p(C_q) ÷ max(outdegree_q, 1). Being cited by a highly-cited paper with few references counts most.
Damping factor d = 0.85: DataRank = (1−d)·B(p) + d·N(p) — the two cards above are each already multiplied by their share.
Self-citations excluded: Citers sharing any OpenAlex author ID with this paper are filtered out before the network sum.

Citers are pulled from OpenAlex sorted by cited_by_count:descand capped per paper, so when the cap binds we keep the highest-signal references and the score is reproducible across reruns.

Read the full methodology →