Affinage

SLBP

Histone RNA hairpin-binding protein · UniProt Q14493

Length
270 aa
Mass
31.3 kDa
Annotated
2026-06-10
29 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLBP is a cell cycle-regulated RNA-binding protein that coordinates the entire post-transcriptional life cycle of replication-dependent histone mRNAs, linking histone biogenesis to S-phase DNA replication and chromatin assembly (PMID:12588979, PMID:15916543). It recognizes the conserved 3' stem-loop through a two-site RNA binding domain—a helix-turn-helix that reads unpaired loop uridines and a second site contacting the stem base—with phosphorylation of a threonine in the intervening TPNK motif increasing affinity by slowing the RNA off-rate while the adjacent proline acts as a hinge orienting the second site (PMID:22439849). In histone pre-mRNA 3' end processing, SLBP is the sole cell cycle-regulated factor required: it restructures the 3'-UTR to expose the histone downstream element for U7 snRNA anchoring, and its processing activity depends both on phosphorylation-coupled folding of the RNA binding/processing domain and on activating ubiquitylation by CRL4(WDR23), which stimulates processing without changing SLBP levels (PMID:12588979, PMID:15260483, PMID:16982637, PMID:27203182). Beyond processing, SLBP travels with histone mRNA into the cytoplasm, where it remains a component of the polyribosomal histone mRNP and promotes translation through the MIF4G-like SLIP1 homodimer; an ordered assembly in which phosphorylated SLBP binds histone mRNA before recruiting SLIP1 generates the active ternary complex, whereas unphosphorylated SLBP forms an inactive high-affinity SLIP1 heterotetramer (PMID:15358832, PMID:23804756, PMID:23286197). SLBP also governs histone mRNA decay: dephosphorylation of the TPNK threonine by PP2A together with Pin1, alongside 3' uridylation by TUT7 and trimming by 3'hExo, cooperatively dissociates SLBP and initiates degradation (PMID:22907757, PMID:37516934). SLBP abundance oscillates through the cell cycle by phosphorylation-triggered, ubiquitin-mediated proteasomal degradation, with SCF–cyclin F targeting SLBP in G2 via a CY motif and FEM1A/B/C–CUL2 complexes contributing degradation at other stages; loss of these degrons abolishes cell cycle oscillation, and stabilized SLBP elevates H2A.X translation and sensitizes cells to genotoxic apoptosis (PMID:12588979, PMID:27773672, PMID:28118078). SLBP function is conserved across animals, including roles in maternal histone mRNA deposition and noncanonical polyadenylated histone mRNA processing in Drosophila oocytes (PMID:33408246, PMID:40239992).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2003 High

    Established that SLBP is the single cell cycle-regulated factor required for histone pre-mRNA 3' end processing and that its level is controlled by phosphorylation-triggered degradation.

    Evidence Mass spectrometry of purified late-S-phase SLBP, degron mutagenesis, and in vitro processing reconstitution with G1/G2 nuclear extracts

    PMID:12588979

    Open questions at the time
    • Did not identify the E3 ligase recognizing the phosphodegron
    • Mechanism by which SLBP enables processing not resolved at this stage
  2. 2004 High

    Defined how phosphorylation enables processing—C-terminal serine phosphorylation cooperates with RNA binding to fold the SLBP RNA binding/processing domain.

    Evidence 31P NMR, circular dichroism, and in vitro processing assays with phosphomimetic mutants in Drosophila SLBP

    PMID:15260483

    Open questions at the time
    • Folding requirement shown in Drosophila SLBP; human equivalence not directly addressed
    • Structural detail of the folded domain not resolved
  3. 2004 Medium

    Showed SLBP accompanies histone mRNA into the cytoplasm as part of the polyribosomal mRNP and relocalizes to the nucleus while staying RNA-binding-active when replication is blocked.

    Evidence Anti-SLBP immunoprecipitation of polyribosome fractions and subcellular fractionation under replication inhibition

    PMID:15358832

    Open questions at the time
    • Did not define the translational machinery SLBP engages
    • Signal driving nuclear relocalization unknown
  4. 2005 Medium

    Linked SLBP function to S-phase progression, demonstrating it is required for efficient DNA replication.

    Evidence RNAi depletion with RNAi-resistant rescue and flow cytometry cell cycle analysis

    PMID:15916543

    Open questions at the time
    • Causal step between histone supply and replication slowing not isolated
    • Chromatin assembly link inferred rather than directly shown
  5. 2006 Medium

    Provided the mechanistic basis for processing—SLBP opens 3'-UTR hairpins to expose the histone downstream element for U7 snRNA.

    Evidence RNA structure probing and EMSA on H4-12 pre-mRNA

    PMID:16982637

    Open questions at the time
    • Did not resolve how U7 anchoring leads to cleavage
    • Other processing factors not mapped onto this rearrangement
  6. 2009 Medium

    Extended SLBP function to nuclear export, showing it is needed for cytoplasmic delivery of fully processed histone mRNA.

    Evidence RNAi knockdown with FISH and cellular fractionation in U2OS cells

    PMID:19155325

    Open questions at the time
    • Export machinery contacted by SLBP not identified
    • Whether export defect is direct or secondary to processing not resolved
  7. 2012 High

    Resolved the two-site architecture of the SLBP RNA binding domain and the kinetic role of TPNK phosphorylation in tightening RNA binding.

    Evidence NMR spectroscopy, kinetic binding assays, and site-directed mutagenesis

    PMID:22439849

    Open questions at the time
    • Co-structure with the stem-loop RNA not determined
    • Did not connect affinity changes to in vivo decay timing
  8. 2012 Medium

    Identified Pin1 and PP2A as regulators that dephosphorylate the TPNK threonine to dissociate SLBP from histone mRNA and control SLBP stability via an N-terminal phosphodegron.

    Evidence Pin1 inhibition/knockdown, in vitro PP2A dephosphorylation, ubiquitination assays, and fractionation

    PMID:22907757

    Open questions at the time
    • E3 ligase acting on the Ser20/Ser23 phosphodegron not identified here
    • Kinase counteracting PP2A not defined
  9. 2013 High

    Defined the structural and ordered-assembly logic of SLBP-driven translation through the SLIP1 homodimer.

    Evidence Crystal structures of zebrafish SLIP1 with SLBP and DBP5 motifs, plus pulldown assays, AUC, ITC, and in vivo mRNA quantification

    PMID:23286197 PMID:23804756

    Open questions at the time
    • How the active ternary complex stimulates ribosome recruitment not shown
    • In vivo phosphorylation switch between heterotetramer and active dimer not directly visualized
  10. 2016 High

    Identified the G2-specific degradation pathway and its physiological consequence—SCF–cyclin F binds SLBP via a CY motif to limit H2A.X translation and genotoxic sensitivity.

    Evidence Reciprocal Co-IP, CY-motif mutagenesis, polyribosome fractionation, and apoptosis assays

    PMID:27773672

    Open questions at the time
    • Did not account for SLBP turnover outside G2
    • Kinase priming the CY-motif-coupled degron not defined
  11. 2016 High

    Revealed a non-degradative ubiquitin signal—CRL4(WDR23) ubiquitylates SLBP to activate processing during S phase without altering its abundance.

    Evidence In vitro and in vivo ubiquitylation, Co-IP, RNAi with processing readouts, and mass spectrometry

    PMID:27203182

    Open questions at the time
    • Ubiquitylated lysines and how they enhance processing not mapped
    • Interplay with phospho-regulation of processing not resolved
  12. 2017 Medium

    Completed the cell cycle degradation network by identifying FEM1A/B/C–CUL2 ligases and showing combined cyclin F and FEM1 degrons are required for SLBP oscillation, with conservation across animals.

    Evidence Co-IP, degron mutagenesis, RNAi in C. elegans, and ortholog Co-IP in C. elegans and Drosophila

    PMID:28118078

    Open questions at the time
    • Cell cycle phases governed by each FEM1 paralog not fully partitioned
    • Signals selecting between FEM1 and cyclin F pathways unknown
  13. 2021 Medium

    Showed a non-processing region of SLBP overlapping its NLS is required for maternal histone mRNA deposition and histone gene transcription in oocytes.

    Evidence Drosophila genetics with deletion/NLS mutants, in situ hybridization, and immunofluorescence

    PMID:33408246

    Open questions at the time
    • Molecular partners mediating deposition not identified
    • Mechanism coupling SLBP to histone transcription not resolved
  14. 2022 Medium

    Placed SLBP expression downstream of a metabolic-epigenetic axis, with 53BP1-ACLY-driven histone acetylation activating the SLBP promoter.

    Evidence Co-IP, ChIP, ACLY activity assay, promoter acetylation analysis, and loss-of-function

    PMID:35037047

    Open questions at the time
    • Direct transcription factors at the SLBP promoter not defined
    • Generality beyond the cell systems tested unclear
  15. 2023 Medium

    Defined the early decay mechanism—uridylation by TUT7 plus TPNK dephosphorylation cooperatively weakens SLBP binding while preserving 3'hExo association.

    Evidence Fluorescence polarization, EMSA, and 1-microsecond molecular dynamics simulations

    PMID:37516934

    Open questions at the time
    • Temporal ordering of uridylation versus dephosphorylation in cells not established
    • Exosome handoff not directly demonstrated
  16. 2025 Medium

    Mapped a direct SLBP-UPF1 interaction in which the SLBP N-terminus restrains UPF1 unwinding yet is required for efficient histone mRNA decay, with UPF2-3'hExo overriding the inhibition.

    Evidence In vitro binding and unwinding assays, cellular decay assays, and contact mapping by mutagenesis (preprint)

    PMID:bio_10.1101_2025.02.23.639735

    Open questions at the time
    • Awaits peer review
    • Structural model of the SLBP-UPF1 complex not resolved at high resolution
  17. 2025 Medium

    Described a noncanonical maternal histone mRNA pathway requiring SLBP but not U7 snRNP, producing polyadenylated transcripts stabilized by cytoplasmic poly(A) elongation.

    Evidence Drosophila genetics with SLBP and U7 snRNP mutants, northern blotting, RNA-seq, and in situ hybridization

    PMID:40239992

    Open questions at the time
    • Factors substituting for U7 snRNP in this pathway not identified
    • Conservation in mammals not addressed
  18. 2025 Low

    Reported a cancer-context role in which SLBP interacts with FADS2 and upregulates SLC7A11 to suppress ferroptosis and drive proliferation.

    Evidence IP-MS, RNA-seq, western blotting, ferroptosis markers, and FADS2-inhibition rescue in lung adenocarcinoma cells

    PMID:41344497

    Open questions at the time
    • No reciprocal validation of the SLBP-FADS2 interaction
    • Cancer cell context may not reflect canonical SLBP function
    • Mechanism linking SLBP to SLC7A11 transcription not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple, partly redundant ubiquitin pathways (cyclin F, FEM1A/B/C, CRL4(WDR23)) and phospho/dephospho cycles are temporally integrated to switch SLBP between processing, translation, and decay functions across a single cell cycle remains unresolved.
  • No unified kinetic model coordinating degron usage with phosphorylation state
  • Kinases setting the TPNK and N-terminal degron phosphorylation not fully identified
  • High-resolution structure of SLBP on the histone stem-loop RNA absent

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 4 GO:0060090 molecular adaptor activity 3 GO:0045182 translation regulator activity 2 GO:0048018 receptor ligand activity 2
Localization
GO:0005634 nucleus 3 GO:0005840 ribosome 2 GO:0005829 cytosol 1
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-392499 Metabolism of proteins 4 R-HSA-8953854 Metabolism of RNA 4
Partners
CCNFFEM1AFEM1BFEM1CPIN1SLIP1UPF1WDR23
Complex memberships
SLBP-SLIP1 ternary complex on histone mRNAhistone mRNP on polyribosomes

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 SLBP is phosphorylated on two threonines (T60 and T61 in a TTP sequence, residues 60-62) in late S phase, as determined by mass spectrometry of purified SLBP, triggering its degradation. Mutation of these residues or a cyclin binding site (aa 99-104) stabilizes SLBP in G2 and mitosis. Nuclear extracts from G1 and G2 cells are deficient in histone pre-mRNA processing, restored by recombinant SLBP, identifying SLBP as the only cell cycle-regulated factor required for histone pre-mRNA processing. Mass spectrometry of purified SLBP from late S-phase cells; site-directed mutagenesis; in vitro pre-mRNA processing assay with nuclear extracts Molecular and cellular biology High 12588979
2009 SLBP knockdown by RNAi results in nuclear retention of properly processed histone mRNA, identifying a role for SLBP in histone mRNA nuclear export. SLBP-depleted cells also show accumulation in S phase and the retained histone mRNA is not rapidly degraded upon inhibition of DNA replication. RNA interference (RNAi) knockdown in U2OS cells; fluorescence in situ hybridization and cellular fractionation to track histone mRNA localization RNA (New York, N.Y.) Medium 19155325
2016 The SCF E3 ubiquitin ligase subunit cyclin F binds SLBP via an atypical CY motif and mediates SLBP ubiquitination and degradation specifically in G2. Mutation of the CY motif prevents G2 degradation. Expression of stable SLBP increases loading of H2AFX mRNA onto polyribosomes, elevating H2A.X levels and sensitizing cells to apoptosis upon genotoxic stress in G2. Co-immunoprecipitation; site-directed mutagenesis of CY motif; polyribosome fractionation; functional apoptosis assays Molecular cell High 27773672
2004 SLBP is a component of the histone mRNP on polyribosomes; histone mRNA from polyribosomes is immunoprecipitated with anti-SLBP antibody. When DNA replication is inhibited, histone mRNA is rapidly degraded but SLBP is relocalized to the nucleus while remaining active for RNA binding and histone pre-mRNA processing. Immunoprecipitation of polyribosome fractions with anti-SLBP; cycloheximide and replication inhibitor treatments with subcellular fractionation Nucleic acids research Medium 15358832
2012 The prolyl isomerase Pin1 regulates SLBP polyubiquitination via the Ser20/Ser23 phosphodegron in the SLBP N-terminus, and Pin1 together with protein phosphatase 2A (PP2A) can dephosphorylate the phosphothreonine in the conserved TPNK sequence of the SLBP RNA binding domain in vitro, dissociating SLBP from histone mRNA. Pin1 inhibition or knockdown increases histone mRNA stability and stabilizes SLBP, causing nuclear accumulation. Chemical inhibition and siRNA knockdown of Pin1; in vitro dephosphorylation assay with PP2A; ubiquitination assays; subcellular fractionation Molecular and cellular biology Medium 22907757
2013 Crystal structure (2.5 Å) of zebrafish SLIP1 bound to the translation-activation domain of SLBP determined. SLIP1 is a MIF4G-like homodimer that contacts SLBP's translation domain. A SLIP1-binding motif (SBM) was also identified in eIF3g and mRNA-export factor DBP5; pulldown assays confirmed SLIP1 binding to both; crystal structure of SLIP1 bound to DBP5 SBM resolved at 3.25 Å. X-ray crystallography (2.5 Å and 3.25 Å structures); pulldown assays Nucleic acids research High 23804756
2017 FEM1A, FEM1B, and FEM1C (CUL2-RING E3 ubiquitin ligase substrate recognition subunits) interact with SLBP via distinct degrons in SLBP's N-terminus and mediate SLBP degradation. An SLBP mutant unable to interact with cyclin F and all three FEM1 proteins fails to oscillate during the cell cycle. FEM1-SLBP interaction is conserved in C. elegans and Drosophila; FEM1 depletion in C. elegans upregulates the SLBP ortholog CDL-1 in oocytes. Co-immunoprecipitation; site-directed mutagenesis of degrons; RNAi in C. elegans; co-immunoprecipitation of orthologs in C. elegans and Drosophila Cell cycle (Georgetown, Tex.) Medium 28118078
2016 The CUL4 E3 ubiquitin ligase complex CRL4(WDR23) binds and ubiquitylates SLBP in vitro and in vivo. This ubiquitylation activates SLBP function in histone mRNA 3' end processing without affecting SLBP protein levels. Loss of CRL4(WDR23) activity causes depletion of histones, inhibited DNA replication, and growth slowdown. In vitro ubiquitylation assay; co-immunoprecipitation; RNAi knockdown with histone mRNA processing readouts; mass spectrometry Molecular cell High 27203182
2012 The SLBP RNA binding domain contains two binding sites for the histone mRNA hairpin: a helix-turn-helix motif (Glu129-Val158) that recognizes unpaired uridines in the loop, and a second site (Arg180-Pro200) recognizing the second G-C base pair from the stem base. Phosphorylation of threonine in the TPNK sequence between the two sites increases SLBP affinity for histone mRNA by slowing the off-rate, while the adjacent proline acts as a hinge for orienting the second binding site. NMR spectroscopy; kinetic binding assays; site-directed mutagenesis Biochemistry High 22439849
2004 Phosphorylation at four C-terminal serine residues (in DTAKDSNSDSDSD) of Drosophila SLBP is necessary for histone pre-mRNA processing. Both serine phosphorylation and RNA binding are required for proper folding of the SLBP RNA binding and processing domain (RPD); neither alone is sufficient. The electrostatic effect of phosphorylation can be partially mimicked by glutamic acid substitutions. 31P NMR; circular dichroism; in vitro pre-mRNA processing assays; site-directed mutagenesis Biochemistry High 15260483
2013 SLIP1 is a homodimer that does not bind RNA; phosphorylated SLBP has weak affinity for SLIP1 (Kd ~3 μM) but unphosphorylated SLBP forms a high-affinity 2:2 heterotetramer with SLIP1 (Kd < 0.9 nM) that cannot bind histone mRNA. Sequential binding—phosphorylated SLBP to histone mRNA followed by SLIP1—is required for an active ternary complex. Phosphorylation at Thr171 promotes dissociation of the inactive heterotetramer to a heterodimer. Mutation near the SLIP1 homodimer interface abolished SLBP interaction in vitro and reduced histone mRNA levels in vivo. Analytical ultracentrifugation; isothermal titration calorimetry; alanine scanning mutagenesis; RNA binding assays; in vivo histone mRNA quantification Biochemistry High 23286197
2006 SLBP binding to histone pre-mRNA induces structural rearrangements in the 3'-UTR that open hairpin structures embedding the histone downstream element (HDE), making the HDE accessible for U7 snRNA anchoring. EMSA demonstrated that SLBP-induced opening of the HDE facilitates U7 snRNA binding to histone H4-12 pre-mRNA. RNA structure probing; electrophoretic mobility shift assay (EMSA) Nucleic acids research Medium 16982637
2005 RNAi depletion of SLBP causes accumulation of cells in S phase and slows S-phase progression after release from a double-thymidine block. Expression of an RNAi-resistant SLBP restores proper S-phase progression, establishing that SLBP is required for efficient DNA replication, likely through its role in chromatin assembly. RNAi knockdown; rescue with RNAi-resistant SLBP; cell cycle analysis by flow cytometry Biochemical Society transactions Medium 15916543
2022 53BP1 functions as a molecular scaffold for nucleoside diphosphate kinase-mediated phosphorylation of ACLY, enhancing ACLY activity. This promotes histone acetylation at the SLBP promoter, driving SLBP transcription. The 53BP1-ACLY-SLBP axis is required for quantitative and qualitative histone biogenesis and genomic integrity. Co-immunoprecipitation; chromatin immunoprecipitation; ACLY activity assay; SLBP promoter acetylation analysis; loss-of-function experiments Nucleic acids research Medium 35037047
2023 Uridylation of the histone mRNA 3' stem-loop by TUT7 weakens SLBP binding affinity (demonstrated by fluorescence polarization and EMSA) while maintaining 3'hExo interactions. Molecular dynamics simulations show that combined uridylation and dephosphorylation of the TPNK motif in SLBP disrupts key RNA-protein interactions, suggesting that trimming by 3'hExo, uridylation, and SLBP dephosphorylation cooperate in the early stages of histone mRNA degradation. Fluorescence polarization; EMSA; 1-μs molecular dynamics simulations RNA biology Medium 37516934
2021 A region of SLBP outside the mRNA-processing domain, overlapping a putative nuclear localization sequence, is required for histone mRNA deposition in the Drosophila oocyte and for histone gene transcription in stage 10B oocytes. SLBP mutants with a 10-amino-acid deletion or mutations in the NLS fail to deposit histone mRNA in the oocyte. Drosophila genetics; SLBP mutant analysis; in situ hybridization; immunofluorescence Journal of cell science Medium 33408246
2025 SLBP directly interacts with the RNA helicase UPF1; the unstructured SLBP N-terminus wraps around the UPF1 helicase core at multiple contact sites. SLBP binding to UPF1 impedes UPF1 unwinding activity, but this interaction is critical for efficient histone mRNA decay in cells because UPF1 unwinding of the stem-loop facilitates degradation by 3'hExo. UPF2 binds 3'hExo and, upon activating UPF1, overrides the inhibitory effect of SLBP. In vitro binding assays; biochemical unwinding assays; cellular decay assays; structural/contact mapping by mutagenesis bioRxivpreprint Medium bio_10.1101_2025.02.23.639735
2025 SLBP interacts with FADS2 (identified by IP-MS) and promotes FADS2 expression. SLBP also transcriptionally upregulates and stabilizes SLC7A11, a ferroptosis suppressor, thereby inhibiting lipid peroxidation and ferroptotic cell death in lung adenocarcinoma cells. SLBP-mediated proliferation is functionally dependent on FADS2, as FADS2 inhibition abrogates SLBP-driven growth. Immunopurification–mass spectrometry (IP-MS); RNA-seq; western blotting; biochemical ferroptosis markers (GSH, MDA, Fe2+); FADS2 inhibition rescue experiments Experimental cell research Low 41344497
2025 In Drosophila, maternal histone mRNAs are polyadenylated with a truncated 3' stem-loop through a noncanonical 3'-end processing mechanism that requires SLBP but not U7 snRNP. These polyadenylated maternal histone transcripts are further stabilized by cytoplasmic poly(A) elongation by Wisp (cytoplasmic poly(A) polymerase), which is required for their translation. Northern blotting; RNA-seq; genetics (SLBP and U7 snRNP mutants); in situ hybridization Nucleic acids research Medium 40239992

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Phosphorylation of stem-loop binding protein (SLBP) on two threonines triggers degradation of SLBP, the sole cell cycle-regulated factor required for regulation of histone mRNA processing, at the end of S phase. Molecular and cellular biology 90 12588979
2009 Knockdown of SLBP results in nuclear retention of histone mRNA. RNA (New York, N.Y.) 81 19155325
2016 Cyclin F-Mediated Degradation of SLBP Limits H2A.X Accumulation and Apoptosis upon Genotoxic Stress in G2. Molecular cell 61 27773672
2004 SLBP is associated with histone mRNA on polyribosomes as a component of the histone mRNP. Nucleic acids research 46 15358832
2012 The prolyl isomerase Pin1 targets stem-loop binding protein (SLBP) to dissociate the SLBP-histone mRNA complex linking histone mRNA decay with SLBP ubiquitination. Molecular and cellular biology 41 22907757
2012 Characterizing the functional consequences of haploinsufficiency of NELF-A (WHSC2) and SLBP identifies novel cellular phenotypes in Wolf-Hirschhorn syndrome. Human molecular genetics 39 22328085
2013 Structural and biochemical studies of SLIP1-SLBP identify DBP5 and eIF3g as SLIP1-binding proteins. Nucleic acids research 32 23804756
2017 FEM1 proteins are ancient regulators of SLBP degradation. Cell cycle (Georgetown, Tex.) 31 28118078
2012 Interaction of the histone mRNA hairpin with stem-loop binding protein (SLBP) and regulation of the SLBP-RNA complex by phosphorylation and proline isomerization. Biochemistry 30 22439849
2019 Knocking down miR-384 promotes growth and metastasis of osteosarcoma MG63 cells by targeting SLBP. Artificial cells, nanomedicine, and biotechnology 27 31007083
2016 CRL4(WDR23)-Mediated SLBP Ubiquitylation Ensures Histone Supply during DNA Replication. Molecular cell 26 27203182
2005 Expression of an RNAi-resistant SLBP restores proper S-phase progression. Biochemical Society transactions 26 15916543
2004 The N-terminal domain of the Drosophila histone mRNA binding protein, SLBP, is intrinsically disordered with nascent helical structure. Biochemistry 19 15260482
2021 DRAIC promotes growth of breast cancer by sponging miR-432-5p to upregulate SLBP. Cancer gene therapy 18 34645975
2004 Electrostatic contribution of serine phosphorylation to the Drosophila SLBP--histone mRNA complex. Biochemistry 13 15260483
2017 Nickel and cadmium-induced SLBP depletion: A potential pathway to metal mediated cellular transformation. PloS one 12 28306745
2013 Assembly of the SLIP1-SLBP complex on histone mRNA requires heterodimerization and sequential binding of SLBP followed by SLIP1. Biochemistry 12 23286197
2006 Binding of human SLBP on the 3'-UTR of histone precursor H4-12 mRNA induces structural rearrangements that enable U7 snRNA anchoring. Nucleic acids research 11 16982637
2021 A region of SLBP outside the mRNA-processing domain is essential for deposition of histone mRNA into the Drosophila egg. Journal of cell science 7 33408246
2019 Abrogation of Stem Loop Binding Protein (Slbp) function leads to a failure of cells to transition from proliferation to differentiation, retinal coloboma and midline axon guidance deficits. PloS one 7 30695021
2014 Contribution of protein phosphorylation to binding-induced folding of the SLBP-histone mRNA complex probed by phosphorus-31 NMR. FEBS open bio 7 25379382
2022 53BP1-ACLY-SLBP-coordinated activation of replication-dependent histone biogenesis maintains genomic integrity. Nucleic acids research 6 35037047
2019 Molecular characterization and expression patterns of stem-loop binding protein (SLBP) genes in protogynous hermaphroditic grouper, Epinephelus coioides. Gene 5 30910559
2025 Maternal histone mRNAs are uniquely processed through polyadenylation in a Stem-Loop Binding Protein (SLBP) dependent manner. Nucleic acids research 4 40239992
2017 Data for the generation of RNA spatiotemporal distributions and interpretation of Chk1 and SLBP protein depletion phenotypes during Drosophila embryogenesis. Data in brief 3 28560279
2025 LINC00885 promotes lung squamous cell carcinoma by upregulating SLBP expression to activate PI3K/Akt pathway. Clinical and experimental medicine 1 41138039
2026 SLBP-independent control of maternal histone mRNA. bioRxiv : the preprint server for biology 0 41542534
2025 SLBP promotes lung adenocarcinoma progression by inhibiting ferroptosis and reprogramming glutamine metabolism via FADS2 interaction. Experimental cell research 0 41344497
2023 Uridylation of the histone mRNA stem-loop weakens binding interactions with SLBP while maintaining interactions with 3'hExo. RNA biology 0 37516934

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