Evidence map›Paper›PMID 38087140›Full record

ArticleBulletin of experimental biology and medicine2023

TFP5, a Peptide Derived from Cdk5 Activator p35, Protects Pancreatic β Cells from Glucose Toxicity.

S-Y Liu, S-L Cao, H-Y Luo, L Bao, J E, B Li, X-M Lan, G-Q Zhang, X Bao, Y-L Zheng

Abstract read
PubMed Publisher
In one paragraph

Article in Bulletin of experimental biology and medicine, 2023. 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
0.6field-weighted citation impact, top 27% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 1 country.

S-Y LiuDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
S-L CaoDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
H-Y LuoDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
L BaoDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
J EDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
B LiDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
X-M LanDepartment of Geriatrics, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
G-Q ZhangDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
X BaoDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China.
Y-L ZhengDepartment of Nephrology, People's Hospital of Ningxia Hui Autonomous Region, Ningxia Medical University, Yinchuan, China. zhengyali@nxmu.edu.cn.
Ningxia Medical University · CNThe Fourth People's Hospital of Ningxia Hui Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We studied the effect of TFP5 on MIN6 cells (cultured mouse islet β cells) treated with different concentrations of glucose (5 or 25 mM). The results were verified in C57BL/6J mice (control; n=12) and db/db mice with type 2 diabetes mellitus (n=12). To synthesize TFP5, peptide p5 (a derivative of p35 protein, activator of cyclin-dependent kinase 5, Cdk5) was conjugated with a FITC tag at the N-terminus and an 11-amino acid TAT protein transduction domain at the C-terminus. TFP5 was employed to inhibit Cdk5 activity and then to evaluate its efficiency in treating experimental type 2 diabetes mellitus. TFP5 effectively inhibited the pathological hyperactivity of Cdk5, enhanced insulin secretion, and protected pancreatic β cells from apoptosis in vitro and in vivo. In addition, TFP5 inhibited inflammation in pancreatic islets by reducing the expression of inflammatory cytokines TGF-β1, TNFα, and IL-1β. These novel data indicates that TFP5 is a promising candidate for treatment of type 2 diabetes mellitus.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsAnimalsCyclin-Dependent Kinase 5GlucoseMiceMice, Inbred C57BLNerve Tissue ProteinsPeptidesCyclin-Dependent Kinase 5GlucoseNerve Tissue Proteinsneuronal Cdk5 activator (p25-p35)PeptidesTFP5 peptideapoptosisCdk5inflammation factorsinsulinTFP5

Identifiers

PMID38087140
OpenAlexW4389684021

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.