ArticleMolecular and cellular biology2001
Functional phosphorylation sites in the C-terminal region of the multivalent multifunctional transcriptional factor CTCF.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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.
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.
Who cites it
50 citing papers in PubMed, 103 citations in OpenAlex.
- SPOP-mediated K27-linked non-degradative ubiquitination of KCNN3 suppressing HCC progression via the CTCF-SATB1 axis.Cell death & disease · 2026Article
- Ectopic Recruitment of the CTCF N-Terminal Domain with Two Proximal Zinc-Finger Domains as a Tool for 3D Genome Engineering.International journal of molecular sciences · 2025Article
- A negatively charged region within carboxy-terminal domain maintains proper CTCF DNA binding.iScience · 2024Article
- The PTM profiling of CTCF reveals the regulation of 3D chromatin structure by O-GlcNAcylation.Nature communications · 2024Article
- Function and Evolution of the Loop Extrusion Machinery in Animals.International journal of molecular sciences · 2023Review
- Cooperation of ATF4 and CTCF promotes adipogenesis through transcriptional regulation.Cell biology and toxicology · 2022Article
- CTCF acetylation at lysine 20 is required for the early cardiac mesoderm differentiation of embryonic stem cells.Cell regeneration (London, England) · 2022Article
- Article
- CTCF and EGR1 suppress breast cancer cell migration through transcriptional control of Nm23-H1.Scientific reports · 2021Article
- Distinct Classes of Chromatin Loops Revealed by Deletion of an RNA-Binding Region in CTCF.Molecular cell · 2019Article
- Article
- Developing in 3D: the role of CTCF in cell differentiation.Development (Cambridge, England) · 2018Review
- O-GlcNAcylation of boundary element associated factor (BEAF 32) in Drosophila melanogaster correlates with active histone marks at the promoters of its target genes.Nucleus (Austin, Tex.) · 2018Article
- The CCCTC-binding factor (CTCF)-forkhead box protein M1 axis regulates tumour growth and metastasis in hepatocellular carcinoma.The Journal of pathology · 2017Article
- Mitotic phosphorylation of CCCTC-binding factor (CTCF) reduces its DNA binding activity.FEBS open bio · 2017Article
- CTCF: making the right connections.Genes & development · 2016Review
- Epigenetic silencing of the XAF1 gene is mediated by the loss of CTCF binding.Scientific reports · 2015Article
- CTCF regulates NELF, DSIF and P-TEFb recruitment during transcription.Transcription · 2015Article
- Tissue-specific insulator function at H19/Igf2 revealed by deletions at the imprinting control region.Human molecular genetics · 2014Article
- Expanding the roles of chromatin insulators in nuclear architecture, chromatin organization and genome function.Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
Abstract
CTCF is a widely expressed and highly conserved multi-Zn-finger (ZF) nuclear factor. Binding to various CTCF target sites (CTSs) is mediated by combinatorial contributions of different ZFs. Different CTSs mediate distinct CTCF functions in transcriptional regulation, including promoter repression or activation and hormone-responsive gene silencing. In addition, the necessary and sufficient core sequences of diverse enhancer-blocking (insulator) elements, including CpG methylation-sensitive ones, have recently been pinpointed to CTSs. To determine whether a posttranslational modification may modulate CTCF functions, we studied CTCF phosphorylation. We demonstrated that most of the modifications that occur at the carboxy terminus in vivo can be reproduced in vitro with casein kinase II (CKII). Major modification sites map to four serines within the S(604)KKEDS(609)S(610)DS(612)E motif that is highly conserved in vertebrates. Specific mutations of these serines abrogate phosphorylation of CTCF in vivo and CKII-induced phosphorylation in vitro. In addition, we showed that completely preventing phosphorylation by substituting all serines within this site resulted in markedly enhanced repression of the CTS-bearing vertebrate c-myc promoters, but did not alter CTCF nuclear localization or in vitro DNA-binding characteristics assayed with c-myc CTSs. Moreover, these substitutions manifested a profound effect on negative cell growth regulation by wild-type CTCF. CKII may thus be responsible for attenuation of CTCF activity, either acting on its own or by providing the signal for phosphorylation by other kinases and for CTCF-interacting protein partners.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.