| 1994 |
B52/SRSF6 (Drosophila ortholog) is an essential gene required for larval development; null mutants are lethal at first and second instar stages, but B52 is not required for splicing of all pre-mRNAs in vivo, indicating tissue/target specificity. |
P-element remobilization to generate null deletion; genetic rescue by germ-line transformation with B52 genomic DNA; RT-PCR of endogenous pre-mRNAs in null larvae |
Molecular and cellular biology |
High |
7935465
|
| 1994 |
B52/SRSF6 functions as both a general splicing factor and a regulator of 5' alternative splice site choice in a concentration-dependent manner in vitro; overexpression in transgenic flies adversely affects development in many cell types, indicating that its concentration is critical in vivo. |
In vitro splicing assays; transgenic fly overexpression; Western blot and whole-mount immunofluorescence |
Molecular and cellular biology |
High |
8035814
|
| 1994 |
B52/SRSF6 colocalizes with RNA polymerase II on polytene chromosomes; its distribution at highly active heat-shock puffs brackets RNA polymerase II, and this distribution depends on transcription levels as shown by UV cross-linking. |
Immunofluorescence on polytene chromosomes; UV cross-linking in nonpolytene cells |
Molecular biology of the cell |
Medium |
8186467
|
| 1995 |
A single amino acid change in the β4 strand of the first RRM of B52/SRSF6 (allele B52ED) acts as a dominant enhancer of RNA-processing defects and alters alternative splice site choice (favoring male-specific doublesex splice), establishing that the RRM1 RNA-binding domain is critical for B52 splicing function in vivo. |
Genetic screen; isolation of dominant and loss-of-function alleles; sequence comparison; in vivo splicing assays at doublesex and white loci |
Molecular and cellular biology |
High |
7565780
|
| 1997 |
B52/SRSF6 binds a specific RNA hairpin loop structure (~20 nt) via both its RRM domains; the RS domain is not required for RNA binding. This was established by SELEX from random RNA pools followed by mutagenesis and enzymatic structure probing. |
SELEX (selection and amplification from random RNA pool); deletion/substitution mutagenesis of RNA; structure-specific enzymatic probing |
Molecular and cellular biology |
High |
9111335
|
| 1998 |
SRp55/SRSF6 specifically binds a 30-nt exonic splicing enhancer (ESE) in avian cardiac troponin T exon 5 with apparent Kd ~60 nM; cooperative binding of at least two SRp55 proteins is required; mutations that alter exon inclusion in vivo correspondingly change SRp55 binding affinity; both purine-rich motifs in the ESE are required. |
Gel mobility retardation (EMSA) with purified SRp55; Hill plot analysis; chemical modification interference (kethoxal, DMS); mutagenesis correlated with in vivo splicing |
RNA (New York, N.Y.) |
High |
9436904
|
| 1999 |
SRp55/SRSF6 does not induce skipping of CD45 exon 4 (unlike SF2/SC35/SRp40/SRp75); antisense inhibition of SRp55 induces exon 4 skipping, and SRp55 expression increases markedly upon T cell activation alongside CD45RA-to-CD45RO isoform switching. |
Overexpression in COS cells; antisense inhibition; flow cytometry for CD45 isoforms; Western blot |
European journal of immunology |
Medium |
10092085
|
| 2000 |
B52/SRSF6 is the predominant SR protein in specific Drosophila tissues (e.g., brain); tissues where B52 is the major SR protein fail to splice the ftz pre-mRNA when B52 is deleted, while other tissues can use alternative SR proteins to substitute, explaining tissue-specific lethality. |
Immunodepletion of B52 from Kc cell nuclear extracts; homologous in vitro splicing assay; immunofluorescence of larval tissues; RT-PCR of ftz mRNA in B52-deletion tissue |
Molecular and cellular biology |
High |
10594020
|
| 2003 |
SRp55/SRSF6 binds an exonic splice enhancer (ESE) in calcitonin exon 4; base changes that decrease SRp55 binding decrease calcitonin splicing in vitro and in vivo; base changes that increase affinity enhance calcitonin mRNA production; SRp55 levels correlate with calcitonin splicing across cell types; SRp55 overexpression stimulates calcitonin mRNA production. |
In vitro splicing assays; binding site mutagenesis; SRp55 overexpression in 293 cells; RT-PCR quantification of calcitonin mRNA |
Biochemistry |
High |
12549914
|
| 2003 |
Human transformer 2β (hTra2β) and SRp55/SRSF6 specifically interact with the calcitonin exon 4 ESE; hTra2β is required for calcitonin splicing in vitro; SRp55 binding to the ESE contributes to calcitonin/CGRP alternative splicing regulation. |
UV cross-linking with HeLa nuclear extract; immunoprecipitation identification of 55-kDa band as SRp55; in vitro splicing assay with hTra2β |
Biochimica et biophysica acta |
Medium |
12531473
|
| 2003 |
Hyperphosphorylation of SRp55/SRSF6 occurs specifically at the RS domain (induced by DRB or overexpression of Clk/Sty) and requires RNA-binding activity; hyperphosphorylated SRp55 relocalizes to enlarged nuclear speckles; Clk/Sty overexpression targets SRp55 for proteasomal degradation via a destabilization signal in the C-terminal 43-aa segment, with the adjacent RS domain critical for Clk/Sty-mediated degradation. |
DRB treatment; Clk/Sty overexpression; phosphorylation mapping; subcellular localization by immunofluorescence; proteasome inhibitor experiments; deletion mutagenesis |
The Biochemical journal |
High |
12549978
|
| 2004 |
SRp55/SRSF6 binds an ESE in the FGFR1 α-exon (identified by UV cross-linking and immunoprecipitation); RNAi-mediated knockdown of SRp55 causes a 6–14-fold decrease in α-exon inclusion, establishing SRp55 as a major regulator of FGFR1 alternative splicing. |
UV cross-linking and immunoprecipitation; RNAi knockdown; RT-PCR quantification of α-exon inclusion; ESE deletion analysis |
Cancer research |
High |
15604250
|
| 2005 |
SRp30c and SRp55/SRSF6 form a heterodimer that binds splicing silencers at the 5' end of tau exons 2 and 10, inhibiting both exons; in exon 2, hTra2β1 binds the inhibitory heterodimer through its RS1 domain; the SRp30c–SRp55 heterodimer may sterically block hTra2β1 binding to a purine-rich enhancer in exon 10. |
Deletion analysis of splicing silencers; protein–protein and protein–RNA binding assays; minigene splicing assays; co-immunoprecipitation of SRp30c–SRp55 complex |
The Journal of biological chemistry |
Medium |
15695522
|
| 2006 |
In Drosophila, B52/SRSF6 acts upstream of the E2F repressor dE2F2 and is required for proper splicing of the de2f2 pre-mRNA; loss of B52 severely reduces dE2F2 protein levels and deregulates dE2F2-dependent gene expression, placing B52 as a specific regulator of the G1/S block. |
Genetic epistasis (de2f1 mutant rescue by B52 loss-of-function); mosaic clonal analysis (S-phase entry assay); intronless de2f2 rescue experiment; RT-PCR of de2f2 splicing in B52-deficient cells |
Molecular and cellular biology |
High |
16611989
|
| 2007 |
B52/SRSF6 regulates alternative splicing of the Drosophila eye-specification gene eyeless, generating two isoforms differing by a 60-aa insert in the paired domain; the long isoform has impaired ability to trigger ectopic eye formation and to bind eyeless target DNA, while overproduction in the eye disc causes a small eye phenotype. |
In vivo splicing analysis; transgenic overexpression of individual isoforms in eye disc; ectopic eye assay; DNA-binding assay in vitro |
PloS one |
High |
17327915
|
| 2007 |
B52/SRSF6 loss or gain of function in the Drosophila developing eye alters splicing profiles of many transcripts involved in brain organogenesis, and B52 (but not dASF/SF2) impairs normal photoreceptor axonal projections and neurogenesis in visual ganglia, demonstrating tissue-specific and target-specific roles. |
Microarray splicing analysis; loss- and gain-of-function in developing eye; phenotypic analysis of ommatidia structure and axonal projections |
Molecular and cellular biology |
Medium |
17283056
|
| 2008 |
SRp55/SRSF6 regulates alternative splicing of KSR1, ZAK, and mda7/IL24, genes involved in apoptosis, as shown by splice-specific microarray analysis upon SRp55 siRNA knockdown; DNA damage in p53-deficient cells alters splicing of Fas toward the anti-apoptotic soluble isoform through changes in splicing activity. |
siRNA knockdown; splice-specific microarray; RT-PCR validation; Western blot for soluble Fas in media |
Gene |
Medium |
18571879
|
| 2008 |
SR proteins ASF/SF2 and SRp55/SRSF6 physically associate with ESEs in tissue factor (TF) exon 5 (at bases 39 and 87–117); weakening either ESE causes severe skipping of TF exon 5 in a minigene reporter system in monocytic cells. |
In silico ESE identification; minigene reporter system; ESE mutagenesis; UV cross-linking/immunoprecipitation confirming physical association |
Journal of thrombosis and haemostasis : JTH |
Medium |
18315555
|
| 2010 |
Drosophila Topoisomerase I (Topo I) associates with and phosphorylates the SR protein B52/SRSF6; expression of a high-affinity B52-binding site in transgenic flies restricts both B52 and Topo I to a single transcription site; B52 RNAi mislocalizes Topo I to the nucleolus; impaired Topo I delivery to a heat shock gene causes mRNA retention at the transcription site and delayed gene deactivation. |
Transgenic binding-site expression; B52 RNAi; co-immunoprecipitation of Topo I–B52; in vitro phosphorylation assay; mRNA FISH; heat shock gene deactivation kinetics |
PLoS genetics |
High |
20862310
|
| 2010 |
SRp40 and SRp55/SRSF6 promote translation of unspliced HIV-1 Gag from intron-containing viral RNA; for SRp40, this activity depends on the second RRM and the RS domain; the effect requires specific nucleotide sequences in the gag-pol coding region (abolished by codon optimization), suggesting SR protein coupling of HIV-1 gRNA biogenesis to translational utilization. |
SR protein overexpression; Gag expression assay; domain deletion mutants; codon-optimized HIV-1 construct |
Journal of virology |
Medium |
20427542
|
| 2010 |
SRp55/SRSF6 inhibits splicing from the 5' splice site of HIV-1 exon 3 by interacting with the GAR splicing enhancer, causing accumulation of partially spliced vpr mRNA; this inhibition requires both the RS domain and RNA-binding domains of SRp55. |
Splicing reporter assays; domain deletion mutants; RT-PCR quantification of HIV-1 mRNA species |
The Journal of biological chemistry |
Medium |
20685659
|
| 2011 |
SRp55/SRSF6 also inhibits splicing from HIV-1 exon 5, generating partially spliced vpu/env mRNAs; inhibition of HIV-1 splicing by SRp55 promotes export of partially spliced mRNAs to the cytoplasm and can induce p24Gag production from a rev-defective provirus. |
Splicing reporter assays; RT-PCR; Western blot for p24Gag; subcellular fractionation |
Virus research |
Medium |
21345357
|
| 2012 |
Dyrk1A interacts with SRp55/SRSF6 and phosphorylates its proline-rich domain; phosphorylation by Dyrk1A suppresses SRp55's ability to promote tau exon 10 inclusion; SRp55 promotes tau exon 10 inclusion through its RS domain (required for subnuclear speckle localization); knockdown of SRp55 promotes exon 10 exclusion. |
Co-immunoprecipitation; in vitro kinase assay; minigene splicing assays; siRNA knockdown; domain deletion (RS domain mutants); immunofluorescence for speckle localization |
The Journal of biological chemistry |
High |
22767602
|
| 2013 |
SRSF6 is amplified and overexpressed in lung and colon cancers; SRSF6 overexpression in immortal lung epithelial cells enhances proliferation, protects from chemotherapy-induced cell death, and confers tumorigenic ability in mice; SRSF6 knockdown inhibits tumorigenicity; SRSF6 up/downregulation alters splicing of tumor suppressors and oncogenes to generate oncogenic isoforms. |
Gene copy number analysis; stable overexpression in lung epithelial cells; proliferation assays; xenograft tumorigenicity; shRNA knockdown; RT-PCR for splice isoforms |
The Journal of pathology |
High |
23132731
|
| 2013 |
SRSF6 directly binds predicted binding sites in the intronic region adjacent to Bim exon 4 (as shown by UV cross-linking followed by Western blotting); mutations in these SRSF6-binding sites abolish BimS mRNA generation from a minigene; zinc-induced hyperphosphorylation of SRSF6 (via cdc2-like kinase) suppresses its binding to the Bim pre-mRNA, promoting exon 4 skipping and preferential BimS production. |
UV cross-linking and Western blot; Bim minigene mutagenesis; RT-PCR; CLK inhibitor (TG003); phosphorylation analysis |
The FEBS journal |
High |
23648111
|
| 2014 |
SRSF6 is a proto-oncogene overexpressed in human skin cancer; transgenic overexpression in mice induces skin hyperplasia and promotes aberrant alternative splicing of 139 target genes including tenascin C; SRSF6 binds alternative exons in tenascin C pre-mRNA, promoting expression of invasive/metastatic cancer isoforms; SRSF6 overexpression depletes LGR6+ stem cells and causes excessive keratinocyte proliferation; effects on wound healing depend on tenascin-C isoforms. |
Transgenic mouse overexpression; RNA-seq for splicing targets; SRSF6 binding to tenascin C exons; skin histology; LGR6+ stem cell quantification; in vitro wound healing assay with isoform rescue |
Nature structural & molecular biology |
High |
24440982
|
| 2015 |
In Drosophila, B52/SRSF6 overexpression increases cell growth (but not differentiation) in the mechanosensory bristle lineage, upregulates myc transcription, and causes loss of thoracic bristles; genetic suppressors identified include upregulation of brat (a post-transcriptional repressor of myc) and downregulation of lilliputian (a superelongation complex subunit). |
Tissue-specific overexpression in bristle lineage; genetic modifier screen; RT-PCR of myc levels; epistasis analysis with brat and lilli |
Genetics |
Medium |
25680814
|
| 2016 |
SRSF6 promotes EMT and metastasis in colorectal cancer cells independently of lncRNA LINC01133; LINC01133 directly binds SRSF6 and inhibits EMT in a manner dependent on SRSF6 presence, acting as a decoy/target mimic. |
Co-IP to identify LINC01133–SRSF6 interaction; SRSF6 knockdown and overexpression; in vitro migration/invasion assays; in vivo metastasis model |
Cancer letters |
Medium |
27443606
|
| 2016 |
RBM4a ablation in brown adipocytes enhances Nova1 exon-4-excluded isoform expression; Nova1 proteins reduce SRSF6 protein levels by promoting inclusion of intron 2 in SRSF6 transcripts (coupled NMD); SRSF6 positively regulates brown adipocyte development, placing it downstream of RBM4a–Nova1 in an AS cascade. |
RBM4a knockout; RNA-seq; RT-PCR of Nova1 and SRSF6 isoforms; Nova1 overexpression; SRSF6 overexpression in adipogenesis assay |
Biochimica et biophysica acta |
Medium |
27535496
|
| 2017 |
SRSF6 regulates ZO-1 exon 23 alternative splicing by directly binding its RNA motif in exon 23, promoting ZO-1 aberrant splicing to drive CRC proliferation and metastasis; the SRSF6 RRM2 domain is key for regulating AS and biological function; indacaterol was identified as an SRSF6 inhibitor targeting RRM2 via virtual screening. |
RIP-seq (RNA immunoprecipitation sequencing); gel shift assay; minigene reporter assay; RRM2 domain deletion analysis; virtual screening; in vitro and in vivo tumor assays |
Gut |
High |
29114070
|
| 2017 |
SRp55/SRSF6 regulates alternative splicing of genes controlling human pancreatic β-cell survival and function, including splicing changes in pro-apoptotic BIM, BAX, JNK signaling components, and ER stress genes; SRp55 depletion triggers β-cell apoptosis and inhibits mitochondrial function/insulin secretion; SRSF6 expression is regulated by the diabetes susceptibility transcription factor GLIS3. |
siRNA knockdown of SRp55 in human β-cells; RNA-seq; apoptosis assays; mitochondrial function assays; insulin secretion assay |
Diabetes |
High |
29246973
|
| 2018 |
B52/SRSF6 increases the splicing efficiency of the temperature-sensitive period (dmpi8) intron in Drosophila; downregulation of B52 in clock neurons increases mid-day siesta and reduces dmpi8 splicing efficiency; natural SNPs in the per 3' UTR modulate B52 binding levels and correlate with sleep behavior variation. |
Cell culture splicing assay; in vivo B52 knockdown in clock neurons; behavioral sleep assay; allele-specific binding analysis |
Scientific reports |
Medium |
29382842
|
| 2018 |
SRSF6 induces inclusion of MYH11 exon 5b in airway smooth muscle cells; siRNA inhibition of SRSF6 reduces SMB isoform expression, establishing SRSF6 as a regulator of smooth muscle myosin heavy chain splicing relevant to asthma. |
Bioinformatics ESE analysis; siRNA knockdown; RT-PCR quantification of SMB isoform |
Physiological reports |
Medium |
30350466
|
| 2020 |
SRSF6 defines a purine-rich (GAA-triplet) consensus RNA-binding motif in human pancreatic β-cells; SRSF6 binds predominantly in coding sequences; binding site position determines splicing outcome; SRSF6 regulates splicing of multiple diabetes susceptibility genes. |
iCLIP (individual-nucleotide resolution UV cross-linking and immunoprecipitation); RNA-seq after SRSF6 knockdown; motif analysis; antisense oligonucleotide modulation of LMO7 splicing |
Life science alliance |
High |
33376132
|
| 2020 |
SRSF6 overexpression in HeLa cells induces alternative splicing changes enriched in DNA damage response and DNA repair pathways; transcriptome analysis confirmed large-scale splicing changes upon SRSF6 overexpression. |
SRSF6 overexpression; RNA-seq; RT-PCR validation of specific AS events |
Oncology reports |
Medium |
32901876
|
| 2020 |
Ablation of SRSF6 in mouse embryonic fibroblasts does not modulate incomplete splicing of HTT exon 1 to exon 2, demonstrating that SRSF6 is not required for this Huntington's disease-associated aberrant splicing event; Srsf6 nullizygosity is embryonic lethal in mice. |
Srsf6 knockout mice; MEF generation; siRNA ablation of SRSF6 in MEFs; RT-PCR for Httexon1 transcript |
Scientific reports |
High |
32820193
|
| 2021 |
CRNDE lncRNA directly binds SRSF6 protein and reduces its protein stability; loss of CRNDE leads to increased SRSF6 activity, which regulates PICALM exon 14 skipping to produce the long PICALM isoform (PICALML), contributing to impaired autophagy flux and chemoresistance in gastric cancer. |
RNA pulldown; co-IP; SRSF6 protein stability assay; minigene splicing assay for PICALM exon 14; autophagy flux assays; PDX model |
Molecular cancer |
High |
33397371
|
| 2021 |
DRAK2 directly binds SRSF6 (co-IP) and inhibits SRSF6 phosphorylation by SRPK1, thereby altering alternative splicing of mitochondrial function-related genes and promoting NASH progression; hepatic deletion of DRAK2 suppresses steatosis-to-NASH progression. |
Co-immunoprecipitation (DRAK2–SRSF6 interaction); phosphoproteome analysis; transcriptome analysis; hepatic DRAK2 conditional knockout; SRPK1 kinase assay in the context of DRAK2 |
Cell metabolism |
High |
34614409
|
| 2022 |
SRSF6 regulates alternative splicing of BAX; loss of SRSF6 promotes accumulation of BAX-κ variant, sensitizing macrophages to cell death and triggering cGAS sensing of cytosolic mitochondrial DNA with upregulation of interferon-stimulated genes; macrophages regulate SRSF6 expression upon pathogen sensing to control mtDNA liberation and programmed cell death threshold. |
SRSF6 loss-of-function in macrophage cell lines; transcriptomic analysis; RT-PCR of BAX isoforms; cGAS sensing assay; apoptosis assays; mtDNA quantification in cytosol |
eLife |
High |
36409059
|
| 2022 |
SRSF6 promotes inclusion of the Fas cassette exon; shRNA knockdown decreases Fas exon inclusion while overexpression increases it; a UGCCAA sequence in the Fas cassette exon is essential for SRSF6 function (identified by deletion and substitution mutagenesis of Fas minigene); SRSF6 interacts with this sequence (biotin-RNA pulldown); 5' splice site strength but not 3' splice site is required for SRSF6-regulated Fas splicing. |
shRNA knockdown; SRSF6 overexpression; Fas minigene deletion/substitution mutagenesis; biotin-labeled RNA pulldown and immunoblotting; splice-site strength mutagenesis |
Cancers |
High |
35454897
|
| 2023 |
SRSF6 levels are strongly reduced under acute hypoxia through inclusion of a poison cassette exon (PCE) promoted by SRSF4; CRISPR/Cas9 removal of the PCE 3' splice site abolishes SRSF6 reduction in hypoxia; reduced SRSF6 drives exon skipping and dispersal of nuclear speckles; aberrantly high SRSF6 in hypoxia attenuates hypoxia-mediated AS, impairs nuclear speckle dispersal, increases proliferation and genomic instability, and suppresses the stress response. |
CRISPR/Cas9 deletion of PCE splice site; SRSF6 overexpression in hypoxia; nuclear speckle imaging; RNA-seq for AS events; proliferation assays; genomic instability assays |
Nucleic acids research |
High |
36620874
|
| 2024 |
SRSF6 regulates the splicing pattern of the histone chaperone HIRA, affecting H3.3 activity; this disrupts AR and E2F oncogenic pathways in prostate cancer cells; SRSF6 modulation affects cell proliferation, migration, colony and tumorsphere formation in vitro and xenograft tumor growth in vivo. |
SRSF6 modulation (knockdown/overexpression); RT-PCR of HIRA isoforms; H3.3 activity assays; AR and E2F pathway readouts; xenograft tumor model |
Science advances |
Medium |
39356765
|
| 2025 |
NSUN2 acts as an m5C 'writer' on SRSF6 mRNA (with ALYREF as 'reader'), stabilizing SRSF6 expression; SRSF6 in turn regulates alternative splicing of UAP1 (redirecting from AGX1 to AGX2 isoform), and AGX2 enhances N-linked glycosylation and stability of ABC transporters, driving multidrug resistance in anaplastic thyroid cancer. |
MeRIP-seq; NSUN2 knockout; transcriptomics; proteomics; nuclear-cytoplasmic fractionation; denaturing IP ubiquitination assay; glycoprotein staining; RT-PCR of UAP1 isoforms; spontaneous ATC mouse model |
Theranostics |
High |
40083919
|
| 2025 |
AGGF1 promotes skipping of SRSF6 exon 3, producing a shorter SRSF6 isoform; full-length SRSF6 overexpression rescues reduced proliferation, migration, and capillary tube formation in AGGF1-silenced endothelial cells; srsf6 knockdown impairs intersomitic vessel development in zebrafish, while overexpression enhances vascular development and partially rescues aggf1 knockdown defects. |
Full-length transcriptome sequencing; AGGF1 siRNA knockdown; SRSF6 isoform overexpression; HPAEC functional assays (proliferation, migration, tube formation); zebrafish srsf6 knockdown and overexpression |
FASEB journal |
Medium |
40035560
|
| 2025 |
SRSF6 and SRSF1 coordinately enhance inclusion of MUSK exon 10 through multiple ESE motifs; SRSF6 exerts a stronger effect than SRSF1 and can compensate for SRSF1 loss; specific functional ESE motifs were defined by mutagenesis; antisense oligonucleotides can switch MUSK isoform expression. |
ESE mutagenesis; SRSF6 and SRSF1 overexpression; SRSF6 knockdown; minigene splicing assay; antisense oligonucleotide experiments |
NAR molecular medicine |
Medium |
40161265
|
| 2026 |
CircNSD2 acts as a scaffold enhancing the interaction between SRSF6 and the deubiquitinase USP10, preventing K48-linked polyubiquitination of SRSF6 at lysine 16 and inhibiting its proteasomal degradation; stabilized SRSF6 reprograms TPM1 alternative splicing to promote TNBC metastasis. |
RNA pulldown; proteomic analysis; RNA immunoprecipitation; co-IP of SRSF6–USP10; ubiquitination assay (denaturing IP); RT-PCR of TPM1 isoforms; in vitro and in vivo metastasis assays |
Molecular cancer |
Medium |
41808072
|
| 2026 |
NMR backbone and sidechain assignments of SRSF6 RRM1 and backbone assignments of pseudo-RRM2 (ΨRRM2) were obtained; secondary structure analysis confirms canonical β1α1β2β3α2β4-fold for each RRM; the inter-domain linker is 37 residues; 15N-relaxation data show the two RRMs tumble as one entity with only transient interaction between them; AlphaFold3 models are largely supported but show subtle inconsistencies at the β4-strand. |
Solution NMR (1H, 13C, 15N backbone/sidechain assignments); 15N-relaxation analysis; secondary chemical shift analysis; comparison with AlphaFold3 models |
Journal of magnetic resonance (San Diego, Calif. : 1997) |
Medium |
42102650
|