Evidence map›Paper›PMID 10982849›Full record

ArticleMolecular and cellular biology2000

Transcriptional regulation of the CLC-K1 promoter by myc-associated zinc finger protein and kidney-enriched Krüppel-like factor, a novel zinc finger repressor.

S Uchida, Y Tanaka, H Ito, F Saitoh-Ohara, J Inazawa, K K Yokoyama, S Sasaki, F Marumo

Open access · greenAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

51 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. EWSR1 rearranged primary renal myoepithelial carcinoma: a diagnostic conundrum.Journal of pathology and translational medicine · 2023
    Article
  6. Review
  7. MiR-181a promotes cell proliferation and migration through targeting KLF15 in papillary thyroid cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Transcription Factor KLF14 and Metabolic Syndrome.Frontiers in cardiovascular medicine · 2020
    Review
  13. Article
  14. Article
  15. Krüppel-like Factor 15: A Potential Therapeutic Target For Kidney Disease.International journal of biological sciences · 2019
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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 2 institutions in 1 country.

S UchidaSecond Department of Internal Medicine, School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan. suchida.med2@med.tmd.ac.jp
Y Tanaka
H Ito
F Saitoh-Ohara
J Inazawa
K K Yokoyama
S Sasaki
F Marumo
Tokyo Medical and Dental University · JPRIKEN · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of CLC-K1 and CLC-K2, two kidney-specific CLC chloride channels, is transcriptionally regulated on a tissue-specific basis. Previous studies have shown that a GA element near their transcriptional start sites is important for basal and cell-specific activities of the CLC-K1 and CLC-K2 gene promoters. To identify the GA-binding proteins, the human kidney cDNA library was screened by a yeast one-hybrid system. A novel member of the Cys2-His2 zinc finger gene designated KKLF (for "kidney-enriched Krüppel-like factor") and the previously isolated MAZ (for "myc-associated zinc finger protein") were cloned. KKLF was found to be abundantly expressed in the liver, kidneys, heart, and skeletal muscle, and immunohistochemistry revealed the nuclear localization of KKLF protein in interstitial cells in heart and skeletal muscle, stellate cells, and fibroblasts in the liver. In the kidneys, KKLF protein was localized in interstitial cells, mesangial cells, and nephron segments, where CLC-K1 and CLC-K2 were not expressed. A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG. In a transient-transfection experiment, MAZ had a strong activating effect on transcription of the CLC-K1-luciferase reporter gene. On the other hand, KKLF coexpression with MAZ appeared to block the activating effect of MAZ. These results suggest that a novel set of zinc finger proteins may help regulate the strict tissue- and nephron segment-specific expression of the CLC-K1 and CLC-K2 channel genes through their GA cis element.

Indexed as

Anion Transport ProteinsGene Expression RegulationMembrane ProteinsNuclear ProteinsPromoter Regions, GeneticTranscription, GeneticAmino Acid SequenceAnimalsBase SequenceCarrier ProteinsChloride ChannelsCloning, MolecularCollagenDisease Models, AnimalDNA-Binding ProteinsDNA, ComplementaryAnion Transport ProteinsCarrier ProteinsChloride ChannelsCLCNKA protein, humanClcnka protein, mouseClcnka protein, ratCLCNKB protein, humanClcnkb protein, mouseClcnkb protein, ratc-MYC-associated zinc finger proteinCollagenDNA-Binding ProteinsDNA, ComplementaryKLF15 protein, humanKruppel-Like Transcription FactorsMembrane ProteinsNuclear ProteinsRecombinant Fusion ProteinsRepressor ProteinsTranscription Factors

Identifiers

PMID10982849
PMCPMC86286
OpenAlexW2163685751

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.