Affinage

HNRNPLL

Heterogeneous nuclear ribonucleoprotein L-like · UniProt Q8WVV9

Round 2 corrected
Length
542 aa
Mass
60.1 kDa
Annotated
2026-04-28
47 papers in source corpus 15 papers cited in narrative 15 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HNRNPLL is an RNA-binding protein that functions as a master regulator of alternative splicing programs during lymphocyte activation, terminal differentiation, and embryonic stem cell lineage commitment. It recognizes CA-rich elements in introns and 3′ UTRs via its RNA-recognition motifs, promoting context-dependent exon inclusion or skipping—most notably silencing CD45 (Ptprc) variable exons upon T cell activation to generate the CD45RO isoform—and stabilizing select mRNAs through 3′ UTR association (PMID:18669861, PMID:25825742, PMID:29869816). Beyond immune cells, HNRNPLL controls pluripotency exit by directing ES cell-preferred exon-skipping events in targets such as Tbx3 and Bptf, and its loss causes developmental defects in knockout mice (PMID:33349972). In cancer, HNRNPLL suppresses colorectal metastasis by repressing CD44v6 splicing and promotes pancreatic cancer invasion through MYOF alternative splicing, illustrating how its splicing targets dictate opposing phenotypic outcomes in different cellular contexts (PMID:28360095, PMID:39742990).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2008 High

    Two independent screens resolved the long-standing question of which trans-acting factor mediates activation-induced CD45 exon skipping in T cells, identifying HNRNPLL as an inducible repressor that binds the ESS1 silencer element and is both necessary and sufficient for the CD45RA-to-CD45RO switch.

    Evidence shRNA screens, overexpression, RNA-binding assays, exon array, and flow cytometry in primary human T cells and cell lines

    PMID:18669861 PMID:18719244

    Open questions at the time
    • Precise structural basis of ESS1 recognition by HNRNPLL RRMs not determined
    • Mechanism by which T cell activation transcriptionally or post-transcriptionally upregulates HNRNPLL not defined
  2. 2008 High

    An ENU point mutation destabilizing the HNRNPLL RRM established that its RNA-binding activity is essential in vivo for a broad alternative splicing program in memory T cells and for peripheral T cell homeostasis, extending its role far beyond a single CD45 target.

    Evidence ENU mutagenesis screen in mice, RRM binding affinity measurement, exon-array profiling of mutant naive and memory T cells

    PMID:19100700

    Open questions at the time
    • Specific splicing targets responsible for the T cell survival defect not fully delineated
    • Whether the peripheral accumulation defect reflects apoptosis, impaired proliferation, or altered homing not resolved
  3. 2012 High

    Demonstration that HNRNPLL regulates immunoglobulin heavy-chain isoform choice and CD44 splicing in plasma cells established it as a shared splicing regulator across both T and B lineage terminal differentiation.

    Evidence Lentiviral shRNA knockdown, RNA immunoprecipitation, RNA-seq, and isoform-specific RT-PCR in plasma cells

    PMID:22991471

    Open questions at the time
    • Mechanism of HNRNPLL-mediated IgH membrane vs. secreted isoform selection not fully characterized
  4. 2014 High

    Deep RNA-seq of Hnrpll-mutant T cells revealed that HNRNPLL induces retention of specific introns flanking alternative exons—not only in Ptprc but in at least 14 other genes—and retroviral rescue of one target (Senp2) partially restored T cell survival, placing a specific downstream effector in the HNRNPLL pathway.

    Evidence Deep sequencing of polyadenylated RNA from Hnrpll-mutant T and B cells; retroviral Senp2 cDNA rescue

    PMID:24476532

    Open questions at the time
    • Whether intron retention is a direct consequence of HNRNPLL binding or a secondary effect is not resolved for most targets
    • Relative contribution of Senp2 versus other targets to the survival phenotype unclear
  5. 2015 High

    PAR-CLIP defined the HNRNPLL binding landscape genome-wide, showing preferential recognition of CA-dinucleotide-rich sequences in introns and 3′ UTRs, and established that 3′ UTR binding stabilizes mRNAs—thereby demonstrating HNRNPLL has dual functions in splicing regulation and mRNA stability during B-to-plasma-cell differentiation.

    Evidence PAR-CLIP in plasma cells, RNA-seq, primary B-to-plasma-cell differentiation assay

    PMID:25825742

    Open questions at the time
    • Structural basis for CA-repeat preference not determined
    • Mechanism by which 3′ UTR binding leads to mRNA stabilization (competition with decay factors?) not elucidated
  6. 2017 Medium

    Identification of PABPC1 as a cytoplasmic interaction partner of HNRNPLL revealed a cooperative mechanism for immunoglobulin mRNA processing: PABPC1 facilitates HNRNPLL binding to IgH transcripts and regulates membrane-to-secreted IgH switching, likely via alternative polyadenylation, while being dispensable for CD45 exon silencing.

    Evidence Co-immunoprecipitation, RNA immunoprecipitation, PABPC1 knockdown, isoform-specific RT-PCR in T cells and plasma cells

    PMID:28611064

    Open questions at the time
    • Whether PABPC1–HNRNPLL interaction is direct or bridged by RNA not established
    • Alternative polyadenylation mechanism inferred but not directly demonstrated
  7. 2017 High

    An in vivo shRNA screen in a colorectal cancer metastasis model showed HNRNPLL suppresses invasion by repressing CD44v6 inclusion; this placed HNRNPLL in cancer biology and demonstrated that its splicing activity on CD44 pre-mRNA has phenotypic consequences for metastasis.

    Evidence Genome-wide shRNA library screen in syngeneic mouse rectal implantation model, RNA-IP, Matrigel invasion, anti-CD44v6 antibody rescue

    PMID:28360095

    Open questions at the time
    • Mechanism linking EMT signals to HNRNPLL downregulation undefined
    • Whether CD44v6 is the sole mediator of metastasis suppression not fully tested
  8. 2018 Medium

    Discovery that ADAR1/2-mediated A-to-I editing of HNRNPLL exon 12A creates an SRSF1-dependent splicing enhancer revealed that HNRNPLL itself is subject to epitranscriptomic regulation, and the resulting E12A isoform controls a distinct set of growth-related genes (CCND1, TGFBR1).

    Evidence RNA-seq, ADAR knockdown/overexpression, splicing reporter, SRSF1 binding analysis, clonogenic and drug sensitivity assays

    PMID:29769310

    Open questions at the time
    • Relative abundance and tissue distribution of E12A isoform not characterized
    • Whether E12A and canonical HNRNPLL have distinct RNA-binding specificities not tested
  9. 2018 Medium

    HNRNPLL was shown to stabilize PCNA, RFC3, and FEN1 mRNAs in colorectal cancer cells, promoting proliferation; epistasis experiments with individual target knockdowns confirmed these as downstream effectors, establishing a pro-proliferative mRNA stability function distinct from its splicing role.

    Evidence RNA-IP, actinomycin D mRNA decay assay, RNA-seq, knockdown epistasis, proliferation assays in CRC cells

    PMID:29869816

    Open questions at the time
    • Whether mRNA stabilization occurs through 3′ UTR CA-element binding (as defined by PAR-CLIP) not confirmed for these specific targets
    • Relevance of this stabilization function in normal (non-cancer) cells untested
  10. 2020 High

    Knockout studies in mice and ES cells revealed that HNRNPLL controls exit from pluripotency by directing ES cell-preferred exon-skipping in Tbx3 and Bptf, extending its biological role beyond the immune system to fundamental developmental cell-fate decisions.

    Evidence HNRNPLL-KO mice, ES cell differentiation assays, RNA-seq alternative splicing analysis

    PMID:33349972

    Open questions at the time
    • Mechanism by which HNRNPLL is upregulated at differentiation onset in ES cells undefined
    • Whether other hnRNP family members compensate partially in KO mice not addressed
  11. 2024 Medium

    HNRNPLL was found to regulate MYOF alternative splicing in pancreatic cancer, promoting the short MYOFb isoform that drives migration and invasion, revealing yet another cancer-relevant splicing target and demonstrating that HNRNPLL can function as a context-dependent pro-metastatic factor.

    Evidence RNA-seq exon-skipping analysis, HNRNPLL knockdown/overexpression, MYOFb rescue, migration and invasion assays in PDAC cell lines

    PMID:39742990

    Open questions at the time
    • Direct binding of HNRNPLL to MYOF pre-mRNA not demonstrated by CLIP
    • In vivo metastasis validation not reported
    • How tissue context determines whether HNRNPLL is pro- or anti-metastatic (CRC vs. PDAC) not mechanistically explained

Open questions

Synthesis pass · forward-looking unresolved questions
  • Unresolved: the structural basis for CA-element recognition, the signaling pathways controlling HNRNPLL induction during activation and differentiation, and the rules determining whether HNRNPLL binding at a given site causes exon inclusion, exon skipping, intron retention, or mRNA stabilization remain undefined.
  • No high-resolution structure of HNRNPLL RRM domains bound to RNA
  • Upstream regulators of HNRNPLL transcription and protein stability largely unknown
  • Decision rules for inclusion vs. skipping vs. stabilization at individual binding sites not modeled

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140098 catalytic activity, acting on RNA 7 GO:0003723 RNA binding 5
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 1
Pathway
R-HSA-8953854 Metabolism of RNA 9 R-HSA-168256 Immune System 6 R-HSA-1266738 Developmental Biology 1
Partners
ADAR1ADAR2PABPC1SRSF1

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 hnRNPLL was identified as a critical inducible regulator of CD45 alternative splicing in T cells. It is up-regulated upon T cell stimulation, binds CD45 pre-mRNA transcripts, and is both necessary and sufficient for activation-induced skipping of CD45 variable exons (generating the CD45RO isoform from CD45RA). Depletion or overexpression in B and T cell lines and primary T cells reciprocally altered CD45RA and RO expression. Exon array analysis indicated hnRNPLL acts as a global regulator of alternative splicing in activated T cells. shRNA interference screen, overexpression, RNA binding assays, exon array analysis, flow cytometry for CD45 isoforms Science High 18669861
2008 A single point mutation in hnRNPLL destabilizes its RNA-recognition domain, which normally binds with micromolar affinity to RNA containing the Ptprc (CD45) exon-silencing sequence. This mutation selectively diminished T cell accumulation in peripheral lymphoid tissues without affecting proliferation, and abrogated the extensive program of alternative mRNA splicing in memory T cells coordinated by hnRNPLL. ENU mutagenesis screen, RRM domain binding assay (micromolar affinity measurement), exon-array analysis of mutant naive and memory T cells Immunity High 19100700
2008 hnRNP LL (hnRNPLL) was identified via a cell-based screen as a distinct signal-induced repressor of CD45 variable exon 4. Its expression and binding to the ESS1 exonic splicing silencer element are up-regulated upon T cell activation. hnRNPLL overexpression increases exon repression; knockdown eliminates activation-induced exon skipping. hnRNPLL has overlapping but distinct binding requirements compared to hnRNP L at ESS1. Cell-based screen for splicing regulators, microarray, overexpression, knockdown, RNA-protein binding assays with ESS1 mutants RNA High 18719244
2012 In plasma cells, hnRNPLL binds Ighg2b mRNA transcripts and promotes an increase in membrane-encoding Ighg2b isoform at the expense of the secreted isoform (opposing ELL2 function). hnRNPLL also alters splicing of CD44 pre-mRNA in plasma cells, promoting variable exon inclusion and decreasing overall CD44 expression. lentiviral shRNA screen, transcriptional profiling, RNA immunoprecipitation, RNA-Seq, isoform-specific RT-PCR PNAS High 22991471
2014 hnRNPLL induces retention of specific introns in polyadenylated mRNA, including introns flanking variable exons 4–6 of Ptprc (CD45). In T cells with an inactivating Hnrpll mutation, these introns are no longer retained. A similar pattern of hnRNPLL-induced differential intron retention flanking alternative exons was identified in 14 other genes. Retroviral re-expression of a normally spliced cDNA of one target, Senp2, partially rescued the survival defect of Hnrpll-mutant T cells, placing Senp2 downstream of hnRNPLL. Deep sequencing of polyadenylated RNA from Hnrpll-mutant T cells and B cells with low Hnrpll; retroviral rescue experiment Genome Biology High 24476532
2015 hnRNPLL preferentially recognizes CA dinucleotide-containing sequences in introns and 3' UTRs of target RNAs in plasma cells (identified by PAR-CLIP). It promotes exon inclusion or exclusion in a context-dependent manner and stabilizes mRNA when associated with 3' UTRs. During B cell to plasma cell differentiation, hnRNPLL mediates a genome-wide switch of RNA processing, leading to loss of Bcl6 expression and increased Ig production. PAR-CLIP (Photoactivatable-Ribonucleoside-Enhanced Cross-Linking and Immunoprecipitation), RNA sequencing, primary B cell to plasma cell differentiation assay PNAS High 25825742
2017 hnRNPLL specifically associates with cytoplasmic poly(A)-binding protein PABPC1 in both T cells and plasma cells (co-immunoprecipitation). PABPC1 is not required for hnRNPLL-mediated alternative splicing of CD45, but promotes hnRNPLL binding to immunoglobulin mRNA and regulates switching from membrane IgH to secreted IgH, likely via mRNA alternative polyadenylation. Co-immunoprecipitation, RNA immunoprecipitation, isoform-specific RT-PCR, knockdown of PABPC1 Journal of Biological Chemistry Medium 28611064
2017 HNRNPLL knockdown enhanced invasion activity of colon cancer cells in vitro and metastatic ability in vivo. RNA immunoprecipitation showed HNRNPLL binds CD44 pre-mRNA; knockdown increased CD44 variable exon 6 (Cd44v6) levels, and a neutralizing CD44v6 antibody suppressed the invasion induced by HNRNPLL knockdown. HNRNPLL expression was down-regulated during EMT, defining a HNRNPLL–CD44v6 axis in colorectal cancer metastasis suppression. Genome-wide shRNA library screen in vivo (rectal implantation syngeneic mouse model), RNA immunoprecipitation, Matrigel invasion assay, neutralizing antibody rescue Gut High 28360095
2018 An alternative HNRNPLL transcript variant containing an additional exon 12A (E12A) is generated by ADAR1/ADAR2-mediated A-to-I RNA editing. ADAR editing of exon 12A creates an enhancer for the splicing factor SRSF1, thereby promoting inclusion of E12A via splicing. The E12A isoform regulates a distinct set of growth-related genes (including CCND1 and TGFBR1) compared to canonical HNRNPLL; silencing E12A impairs clonogenic ability and enhances sensitivity to doxorubicin. RNA-seq, ADAR knockdown/overexpression, splicing reporter assays, SRSF1 binding analysis, clonogenic assay, drug sensitivity assay Journal of Biological Chemistry Medium 29769310
2018 HNRNPLL stabilizes mRNAs encoding DNA replication factors PCNA, RFC3, and FEN1 in colorectal cancer cells, promoting cell cycle progression and proliferation. RNA immunoprecipitation demonstrated direct binding of HNRNPLL to these mRNAs. HNRNPLL overexpression suppressed actinomycin D-induced degradation of these transcripts, and knockdown of any single target (PCNA, RFC3, or FEN1) suppressed the proliferative effect of HNRNPLL overexpression. RNA immunoprecipitation, actinomycin D mRNA stability assay, RNA-seq, knockdown epistasis experiments, cell proliferation assay Cancer Science Medium 29869816
2020 hnRNPLL controls exit from pluripotency in embryonic stem cells by promoting ES cell-preferred exon skipping events upon onset of differentiation. hnRNPLL depletion leads to sustained expression of ES cell-preferred isoforms of Bptf and Tbx3, causing differentiation deficiency, developmental defects, and growth impairment in hnRNPLL-KO mice. Bioinformatic screening combined with functional RBP knockdown/knockout, alternative splicing analysis by RNA-seq, hnRNPLL knockout mice The EMBO Journal High 33349972
2011 hnRNPLL acts as a trans-acting factor required for alternative splicing of the Ptprc mRNA (silencing of CD45 RA, RB, and RC exons) in both conventional T cells and NKT cells equally. However, hnRNPLL is required for survival of conventional T cells but not NKT cells, revealing divergent functions beyond splicing regulation. Analysis of Hnrpllthunder point mutation in mice, flow cytometry, CD45 isoform analysis by RT-PCR, cell number and functional assays in NKT vs conventional T cells PLoS ONE Medium 22073166
2021 In plasmablasts, hnRNPLL mutation disrupts alternative splicing of Ptprc, preventing downregulation of B220 (high-molecular-weight CD45 isoforms persist). However, this dysregulation of Ptprc splicing does not affect B cell development, mature B cell subsets, B cell proliferation, or in vitro plasmablast generation. The germinal center B cell defect in Hnrnpllthu/thu mice is B cell extrinsic. Mixed bone marrow chimera analysis, in vitro B cell stimulation and differentiation assays, CD45 isoform analysis, immunization experiments Immunology and Cell Biology Medium 33331104
2023 A lncRNA (lnc-PPP2R1B) physically interacts with and stabilizes HNRNPLL protein. This interaction promotes HNRNPLL-mediated alternative splicing of PPP2R1B pre-mRNA, retaining exons 2 and 3, which preserves PP2A enzyme function, enhances dephosphorylation and nuclear translocation of β-catenin, and thereby promotes osteogenesis of mesenchymal stem cells. RNA immunoprecipitation, lncRNA overexpression/knockdown, HNRNPLL knockdown, alternative splicing analysis, PP2A activity assay, β-catenin nuclear translocation assay, in vivo ectopic osteogenesis Stem Cell Reviews and Reports Medium 37243830
2024 hnRNPLL regulates alternative splicing of myoferlin (MYOF) pre-mRNA in pancreatic ductal adenocarcinoma. hnRNPLL depletion stimulates MYOF exon 17 retention, reducing production of the short MYOF isoform (MYOFb) and inhibiting cancer cell migration and invasion. Overexpression of hnRNPLL or MYOFb promoted pancreatic cancer cell migration and invasion, placing MYOFb downstream of hnRNPLL in promoting early metastasis. RNA-seq (exon skipping analysis), hnRNPLL knockdown/overexpression, MYOFb overexpression rescue, migration and invasion assays Cancer Letters Medium 39742990

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Insights into RNA biology from an atlas of mammalian mRNA-binding proteins. Cell 1718 22658674
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
2012 The mRNA-bound proteome and its global occupancy profile on protein-coding transcripts. Molecular cell 973 22681889
2005 Nucleolar proteome dynamics. Nature 934 15635413
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2006 A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration. Cell 610 16713569
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2016 Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing. Cell 423 26871637
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2011 Next-generation sequencing to generate interactome datasets. Nature methods 200 21516116
2008 Regulation of CD45 alternative splicing by heterogeneous ribonucleoprotein, hnRNPLL. Science (New York, N.Y.) 169 18669861
2020 UFMylation maintains tumour suppressor p53 stability by antagonizing its ubiquitination. Nature cell biology 168 32807901
2020 Synthetic Lethal and Resistance Interactions with BET Bromodomain Inhibitors in Triple-Negative Breast Cancer. Molecular cell 159 32416067
2017 Mammalian APE1 controls miRNA processing and its interactome is linked to cancer RNA metabolism. Nature communications 99 28986522
2012 Charting the landscape of tandem BRCT domain-mediated protein interactions. Science signaling 92 22990118
2017 Cell cycle-dependent phosphorylation regulates RECQL4 pathway choice and ubiquitination in DNA double-strand break repair. Nature communications 89 29229926
2004 Analysis of a high-throughput yeast two-hybrid system and its use to predict the function of intracellular proteins encoded within the human MHC class III region. Genomics 87 14667819
2008 A cell-based screen for splicing regulators identifies hnRNP LL as a distinct signal-induced repressor of CD45 variable exon 4. RNA (New York, N.Y.) 84 18719244
2010 Nuclear import of histone deacetylase 5 by requisite nuclear localization signal phosphorylation. Molecular & cellular proteomics : MCP 83 21081666
2020 Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains. Cell reports 79 32814053
2022 SARS-CoV-2 N Protein Antagonizes Stress Granule Assembly and IFN Production by Interacting with G3BPs to Facilitate Viral Replication. Journal of virology 75 35652658
2019 The midbody interactome reveals unexpected roles for PP1 phosphatases in cytokinesis. Nature communications 74 31586073
2008 Memory T cell RNA rearrangement programmed by heterogeneous nuclear ribonucleoprotein hnRNPLL. Immunity 73 19100700
2017 HNRNPLL, a newly identified colorectal cancer metastasis suppressor, modulates alternative splicing of CD44 during epithelial-mesenchymal transition. Gut 62 28360095
2015 RNA-binding protein hnRNPLL regulates mRNA splicing and stability during B-cell to plasma-cell differentiation. Proceedings of the National Academy of Sciences of the United States of America 49 25825742
2014 The RNA-binding protein hnRNPLL induces a T cell alternative splicing program delineated by differential intron retention in polyadenylated RNA. Genome biology 46 24476532
2012 Heterogeneous nuclear ribonucleoprotein L-like (hnRNPLL) and elongation factor, RNA polymerase II, 2 (ELL2) are regulators of mRNA processing in plasma cells. Proceedings of the National Academy of Sciences of the United States of America 35 22991471
2017 Cytoplasmic poly(A)-binding protein 1 (PABPC1) interacts with the RNA-binding protein hnRNPLL and thereby regulates immunoglobulin secretion in plasma cells. The Journal of biological chemistry 27 28611064
2018 Tumor-associated intronic editing of HNRPLL generates a novel splicing variant linked to cell proliferation. The Journal of biological chemistry 20 29769310
2020 hnRNPLL controls pluripotency exit of embryonic stem cells by modulating alternative splicing of Tbx3 and Bptf. The EMBO journal 15 33349972
2018 HNRNPLL stabilizes mRNA for DNA replication proteins and promotes cell cycle progression in colorectal cancer cells. Cancer science 12 29869816
2016 RNA-binding protein hnRNPLL as a critical regulator of lymphocyte homeostasis and differentiation. Wiley interdisciplinary reviews. RNA 11 26821996
2023 Lnc-PPP2R1B Mediates the Alternative Splicing of PPP2R1B by Interacting and Stabilizing HNRNPLL and Promotes Osteogenesis of MSCs. Stem cell reviews and reports 8 37243830
2011 Differential requirement for the CD45 splicing regulator hnRNPLL for accumulation of NKT and conventional T cells. PloS one 8 22073166
2021 Loss of hnRNPLL-dependent splicing of Ptprc has no impact on B-cell development, activation and terminal differentiation into antibody-secreting cells. Immunology and cell biology 7 33331104
2024 hnRNPLL regulates MYOF alternative splicing and correlates with early metastasis in pancreatic ductal adenocarcinoma. Cancer letters 5 39742990
2020 Behavioural phenotyping of thunder mice with a hypomorphic mutation of heterogeneous nuclear ribonuclear protein L-like (hnRNPLL) and reduced T cell function. Neuroscience letters 2 33152455
2026 Integrative Multi-Omics Analysis Reveals HNRNPLL as a Potential Biomarker Associated with Hepatocellular Carcinoma Progression. Metabolites 0 42042880