Affinage

BRSK2

Serine/threonine-protein kinase BRSK2 · UniProt Q8IWQ3

Length
736 aa
Mass
81.6 kDa
Annotated
2026-06-09
35 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BRSK2 (SAD-A) is an AMPK-related serine/threonine kinase that operates as a downstream effector of multiple upstream activating signals to control neuronal polarity, regulated secretion, and stress-adaptive cell survival (PMID:18854318, PMID:30307479, PMID:22669945). It is activated by LKB1 phosphorylation in cell-free systems independently of LKB1 Ser-431 status (PMID:18854318), by PKA via Thr260 (PMID:16870137), and is held in check by an autoinhibitory phosphosite at Thr443 (PMID:23629625); its abundance is further gated by mTORC1-dependent translation of a structured 5'-UTR (PMID:23922392). In neurons, BRSK2 localizes to synaptic vesicles and the presynaptic cytomatrix through a C-terminal short conserved region, phosphorylates the active-zone protein RIM1, and regulates neurotransmitter release and the readily releasable pool (PMID:16630837), while in vivo it is required for cortical radial migration, lamination, and axon outgrowth (PMID:30307479). In pancreatic β-cells BRSK2 couples glucose and incretin (GLP-1/cAMP) cues to insulin exocytosis by directly phosphorylating a set of substrates that drive cytoskeletal remodeling and Rho-GTPase mobilization—PAK1 at Thr423 (PMID:22669945), GDIα at Ser174 to release Rho GTPases (PMID:29873699), and PCTAIRE1/CDK16 at Ser12 (PMID:22798068)—and by phosphorylating Bad at Ser155 to limit lipotoxic apoptosis (PMID:30573363); genetic studies establish that BRSK2 is essential for normal glucose- and incretin-stimulated insulin secretion yet, when stabilized under lipid overload, drives basal hyperinsulinemia and insulin resistance (PMID:23922392, PMID:23629625, PMID:37188647). BRSK2 protein levels are tightly controlled by APC/C(Cdh1)-mediated KEN-box-dependent ubiquitin-proteasome degradation (PMID:23029325) and by Jab1/CSN5 (PMID:22609399). In cancer and nutrient-stress contexts BRSK2 phosphorylates TSC2 to suppress mTORC1 (PMID:28591720), suppresses NRF2 by driving AMPK and inhibiting mTOR-dependent protein synthesis (PMID:32546533), phosphorylates PIMREG at Ser16 to promote its degradation and restrain NF-κB signaling (PMID:38582395), and associates with the Vps34–Beclin-1–ATG14 complex to sustain stress-induced autophagy and survival (PMID:41258112); a potent cell-active inhibitor, GW296115, blocks BRSK2-driven signaling (PMID:32985588).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2006 High

    Established BRSK2's presynaptic function: it was unknown how SAD kinases act at the synapse, and this work placed BRSK2 on synaptic vesicles and the active zone where it phosphorylates RIM1 to govern transmitter release.

    Evidence Subcellular fractionation, immunolocalization, electrophysiology and in vitro kinase assay in hippocampal neurons

    PMID:16630837

    Open questions at the time
    • Whether RIM1 phosphorylation is the sole release-relevant substrate is not resolved
    • In vivo neuronal consequence not addressed in this study
  2. 2006 Medium

    Identified a second activating input: PKA was shown to phosphorylate BRSK2 at Thr260 and bind it, linking cAMP signaling to BRSK2 activity.

    Evidence In vitro kinase assay, GST pull-down, Thr260 mutagenesis

    PMID:16870137

    Open questions at the time
    • Single-lab in vitro evidence
    • Cellular and physiological relevance of Thr260 not tested here
  3. 2008 High

    Defined the upstream activating kinase: BRSK2 activation by LKB1 was reconstituted in vitro and shown to be independent of LKB1 Ser-431, clarifying the activation hierarchy.

    Evidence Cell-free kinase assay with recombinant STRADα·MO25α·LKB1 and BRSK2; HeLa co-expression

    PMID:18854318

    Open questions at the time
    • Activation loop site phosphorylated by LKB1 not specified here
    • Physiological context of LKB1-BRSK2 axis not addressed
  4. 2012 High

    Connected BRSK2 to insulin secretion machinery via direct substrates: identification of PCTAIRE1 (Ser12) and PAK1 (Thr423) as BRSK2 targets revealed how the kinase modulates GSIS and cytoskeletal remodeling.

    Evidence Yeast two-hybrid, GST pull-down, co-IP, in vitro kinase, siRNA in MIN6/β-cells, in vivo insulin measurements

    PMID:22669945 PMID:22798068

    Open questions at the time
    • Opposing functional effects (PCTAIRE1 suppresses vs PAK1 promotes GSIS) not fully reconciled
    • Stoichiometry and timing of substrate phosphorylation during secretion unknown
  5. 2012 High

    Revealed how BRSK2 abundance is controlled in the cell cycle: APC/C(Cdh1) degrades BRSK2 via a KEN box, and Jab1/CSN5 promotes its proteasomal turnover, coupling kinase levels to mitotic progression.

    Evidence Immunofluorescence, cell-cycle synchronization, ubiquitination assays, Cdh1 and Jab1 knockdown, flow cytometry

    PMID:22609399 PMID:23029325

    Open questions at the time
    • Functional purpose of mitotic centrosomal BRSK2 not defined
    • Jab1 mechanism relative to APC/C(Cdh1) not integrated
  6. 2012 Low

    Probed BRSK2 in proteostasis: ER stress relocalizes and downregulates BRSK2, and a kinase-independent anti-apoptotic activity plus VCP/p97-associated ERAD function were proposed.

    Evidence Western blot, subcellular localization, knockdown/overexpression (WT and kinase-dead), co-IP and domain mapping with VCP/p97

    PMID:22713462 PMID:23907667

    Open questions at the time
    • VCP/p97 link rests on single co-IP with indirect ERAD readout
    • Kinase-independent anti-apoptotic mechanism unexplained
    • Not independently confirmed
  7. 2013 High

    Placed BRSK2 within nutrient and incretin signaling in β-cells: glucose- and mTORC1-dependent translation controls SAD-A levels, and GLP-1/cAMP/Ca2+ activates it via relief of Thr443 autoinhibition, establishing it as required for GSIS and incretin action.

    Evidence Conditional/global knockout mice, glucose tolerance tests, rapamycin, 5'-UTR reporters, Thr443 mutagenesis, islet secretion assays

    PMID:23629625 PMID:23922392

    Open questions at the time
    • Kinase responsible for Thr443 phosphorylation not identified
    • Link between mTORC1-driven translation and acute secretion timing unclear
  8. 2017 Medium

    Defined a survival-promoting BRSK2 arm in cancer: BRSK2 phosphorylates TSC2 to suppress mTORC1 under nutrient deprivation, relieving feedback inhibition on Akt.

    Evidence Western blot for pTSC2/mTORC1 substrates, nutrient deprivation, overexpression/knockdown in PDAC cells

    PMID:28591720

    Open questions at the time
    • Direct TSC2 phosphosite not mapped
    • Single-lab; in vivo tumor relevance not tested
  9. 2018 Medium

    Extended the β-cell secretory mechanism: BRSK2 phosphorylates GDIα at Ser174 to release Rho GTPases and drives Bad Ser155 phosphorylation, coupling exocytosis to anti-apoptotic protection downstream of GLP-1.

    Evidence Co-IP, in vitro kinase/phosphorylation assay, shRNA, insulin secretion assays in INS-1 and primary islets; pBad-S155 blots and apoptosis assays

    PMID:29873699 PMID:30573363

    Open questions at the time
    • Direct Bad phosphorylation not confirmed by in vitro kinase assay
    • Which Rho GTPases are mobilized downstream not delineated
  10. 2019 High

    Established BRSK2's developmental role in vivo: Sada-/- mice show disorganized cortical lamination, delayed radial migration, and shortened axons, defining BRSK2 as essential for cortical neuron migration and polarization.

    Evidence Knockout mice, BrdU birthdating, in utero electroporation with time-lapse imaging, hippocampal neuron morphometry

    PMID:30307479

    Open questions at the time
    • Substrates mediating migration/polarization in vivo not identified
    • Relationship to presynaptic RIM1 function unresolved
  11. 2020 Medium

    Connected BRSK2 kinase activity to redox and translational control: BRSK2 drives AMPK and suppresses mTOR, reducing protein synthesis and NRF2 levels.

    Evidence Gain-of-function kinase screen, phosphoproteomics, RNAseq, NRF2 reporter, kinase-dead controls

    PMID:32546533

    Open questions at the time
    • Direct AMPK/mTOR-axis substrates of BRSK2 not pinpointed
    • Single-lab activity-overexpression context
  12. 2020 Medium

    Provided a chemical-biology tool: GW296115 was characterized as a potent, cell-active BRSK2 inhibitor enabling target engagement studies.

    Evidence KINOMEscan profiling of 403 kinases, cellular thermal shift assay, downstream phospho-westerns

    PMID:32985588

    Open questions at the time
    • Off-target activity across the kinome not exhaustively excluded
    • In vivo pharmacology not established
  13. 2023 High

    Reframed BRSK2 in metabolic disease: lipid-induced BRSK2 stabilization drives kinase-dependent basal insulin hypersecretion, and β-cell knockout protects from HFD-induced hyperinsulinemia and insulin resistance.

    Evidence Inducible β-cell-specific knockout and gain-of-function mice, HFD feeding, kinase-dead mutant, insulin secretion assays

    PMID:37188647

    Open questions at the time
    • Molecular basis of lipid-induced BRSK2 stabilization not defined
    • Lipid-sensing substrate(s) driving basal secretion not identified
  14. 2024 Medium

    Linked BRSK2 to inflammatory signaling in cancer: BRSK2 phosphorylates PIMREG at Ser16 to promote its degradation and limit NF-κB, and its loss confers cisplatin resistance.

    Evidence miR-3960 overexpression, BRSK2 knockdown/rescue, Ser16-PIMREG phosphorylation and ubiquitination assays, NF-κB reporter, cisplatin resistance assays in TNBC

    PMID:38582395

    Open questions at the time
    • E3 ligase acting on PIMREG not identified
    • Single-lab; direct kinase assay on PIMREG not shown
  15. 2025 Medium

    Implicated BRSK2 in autophagy-driven cancer survival: endogenous BRSK2 associates with the Vps34-Beclin-1-ATG14 complex and sustains basal and stress autophagy plus AKT/STAT3/NF-κB survival signaling.

    Evidence Co-IP with autophagy complex components, siRNA, GW296115, autophagy flux and survival/metastasis assays

    PMID:41258112

    Open questions at the time
    • Whether association is direct and which subunit is the kinase substrate unknown
    • Single-lab co-IP without reciprocal structural validation

Open questions

Synthesis pass · forward-looking unresolved questions
  • How BRSK2's diverse substrate sets and contexts (presynaptic RIM1, β-cell secretory machinery, mTOR/NRF2/NF-κB stress nodes, autophagy complex) are coordinated by upstream activation and degradation in a single integrated regulatory logic remains unresolved.
  • No unified model linking tissue-specific substrate selection to upstream LKB1/PKA/mTORC1 inputs
  • Activation-loop phosphosite and full activation mechanism not consolidated
  • In vivo substrate specificity in cancer contexts not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0016740 transferase activity 4 GO:0098772 molecular function regulator activity 2
Localization
GO:0005783 endoplasmic reticulum 1 GO:0005815 microtubule organizing center 1 GO:0005886 plasma membrane 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-112316 Neuronal System 2 R-HSA-162582 Signal Transduction 2 R-HSA-392499 Metabolism of proteins 2 R-HSA-1266738 Developmental Biology 1 R-HSA-1640170 Cell Cycle 1 R-HSA-9612973 Autophagy 1
Partners
BECLIN-1CDK16GDIΑJAB1/CSN5LKB1PAK1PRKACAVCP
Complex memberships
Vps34-Beclin-1-ATG14 autophagy complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 SAD-B (BRSK2 paralog; this paper characterizes SAD-A/SAD-B as mammalian orthologs) localizes to synaptic vesicles and the presynaptic cytomatrix via a short conserved region (SCR) in the C-terminus; overexpression increases miniature EPSC frequency; introduction of SCR into presynaptic neurons inhibits evoked synaptic transmission and reduces the readily releasable pool; SAD-B directly phosphorylates active zone protein RIM1 but not Munc13-1. Subcellular fractionation, immunolocalization, electrophysiology in cultured hippocampal neurons, hypertonic sucrose RRP assay, in vitro kinase assay Neuron High 16630837
2008 LKB1 phosphorylates and activates BRSK2 (and BRSK1) in cell-free assays; C-terminal phosphorylation of LKB1 at Ser-431 is NOT required for this activation — all LKB1 variants (S431A, S431E, LKB1S) are equally effective at phosphorylating and activating BRSK2. Cell-free kinase assay with recombinant STRADα·MO25α·LKB1 complexes and recombinant BRSK1/BRSK2 substrates; co-expression in HeLa cells The Journal of biological chemistry High 18854318
2006 PKA phosphorylates BRSK2 at Thr260 and increases its kinase activity; PKA physically associates with BRSK2 as shown by GST pull-down. In vitro kinase assay, GST pull-down, site-directed mutagenesis (Thr260) Biochemical and biophysical research communications Medium 16870137
2012 BRSK2 interacts with PCTAIRE1 (CDK16) via yeast two-hybrid, GST pull-down, and co-immunoprecipitation; BRSK2 phosphorylates PCTAIRE1 at Ser-12; this phosphorylation reduces glucose-stimulated insulin secretion (GSIS) in MIN6 β-cells; BRSK2 knockdown increases serum insulin in mice. Yeast two-hybrid, GST pull-down, co-immunoprecipitation, in vitro kinase assay, siRNA knockdown in MIN6 cells, in vivo mouse insulin measurements The Journal of biological chemistry High 22798068
2012 SAD-A (BRSK2) directly binds PAK1 through its kinase domain; the interaction is mediated by the p21-binding domain (PBD) of PAK1 and requires both kinases in active conformations; SAD-A directly phosphorylates PAK1 at Thr-423, triggering the onset of GSIS; overexpression of SAD-A stimulates cytoskeletal remodeling required for insulin exocytosis. Co-immunoprecipitation, in vitro kinase assay, siRNA/dominant-negative constructs, insulin secretion assay, cytoskeletal remodeling assay The Journal of biological chemistry High 22669945
2013 Global SAD-A deletion leads to defective GSIS and small islets; SAD-A protein translation is stimulated by glucose and inhibited by rapamycin, placing it as a downstream effector of mTORC1 signaling; the highly structured 5'-UTR of SAD-A mRNA requires mTORC1 for translation initiation. Conditional knockout mice, glucose tolerance tests, islet morphometry, rapamycin treatment, 5'-UTR reporter constructs Proceedings of the National Academy of Sciences of the United States of America High 23922392
2012 BRSK2 co-localizes with centrosomes during mitosis; BRSK2 protein levels peak during mitosis and decline in G1; APC/C(Cdh1) targets BRSK2 for ubiquitin-proteasome degradation via a KEN box motif; Cdh1 (not Cdc20) promotes this degradation; BRSK2 overexpression (WT or ΔKEN) increases the G2/M fraction. Immunofluorescence, cell cycle synchronization, co-immunoprecipitation, ubiquitination assay, Cdh1 knockdown, flow cytometry PloS one High 23029325
2012 Jab1 (CSN5) directly interacts with BRSK2 (GST pull-down and co-IP); Jab1 promotes ubiquitination and proteasome-dependent degradation of BRSK2; Jab1 silencing increases cellular BRSK2 levels; exogenous Jab1 reverses BRSK2-mediated G2/M arrest. GST pull-down, co-immunoprecipitation, ubiquitination assay, siRNA knockdown, cell cycle analysis Biochemical and biophysical research communications Medium 22609399
2013 SAD-A (BRSK2) is activated in response to GLP-1 through cAMP/Ca2+-dependent signaling pathways; conditional pancreatic deletion of SAD-A impairs incretin's effect on GSIS; Thr443 is identified as a key autoinhibitory phosphorylation site — ablation of Thr443 enhances GLP-1's effect on GSIS. Conditional knockout mice, glucose tolerance test, GLP-1 stimulation assays, site-directed mutagenesis (Thr443), isolated islet secretion assay Molecular and cellular biology High 23629625
2012 ER stress down-regulates BRSK2 protein levels and relocalizes endogenous BRSK2 to the ER; BRSK2 knockdown enhances ER stress-mediated apoptosis (increased CHOP and cleaved caspase-3), while BRSK2 overexpression (both WT and kinase-dead) reduces apoptosis, suggesting a kinase-independent anti-apoptotic role. Western blotting, immunofluorescence/subcellular localization, siRNA knockdown, overexpression (WT and kinase-dead), RT-PCR for CHOP Biochemical and biophysical research communications Medium 22713462
2013 BRSK2 interacts with VCP/p97 via three of its four functional domains; BRSK2 affects VCP/p97 activity in ER-associated degradation (ERAD); BRSK2 knockdown increases levels of CD3δ, an ERAD substrate of VCP/p97; BRSK2 and VCP/p97 co-localize by immunofluorescence. Co-immunoprecipitation, domain-mapping assays, siRNA knockdown, immunofluorescence Biotechnology letters Low 23907667
2017 BRSK2, induced by nutrient deprivation in pancreatic cancer cells, phosphorylates TSC2, suppressing mTORC1 activity; reduced mTORC1 signaling eliminates feedback inhibition on Akt, enhancing cell survival under energy deprivation. Western blotting for pTSC2 and mTORC1 substrates, nutrient deprivation assays, BRSK2 overexpression/knockdown in PDAC cells Oncotarget Medium 28591720
2018 SAD-A (BRSK2) directly binds GDIα through its kinase domain and phosphorylates GDIα at Ser174, causing dissociation of Rho GTPases from GDIα complexes and promoting insulin exocytosis; GLP-1 potentiates this phosphorylation; SAD-A deficiency (shRNA) reduces endogenous GDIα Ser174 phosphorylation. Co-immunoprecipitation, in vitro kinase/phosphorylation assay, shRNA knockdown, insulin secretion assay in INS-1 cells and primary islets Endocrinology High 29873699
2018 SAD-A (BRSK2) promotes phosphorylation of Bad at Ser155 downstream of GLP-1/cAMP signaling; SAD-A knockdown exacerbates β-cell dysfunction and apoptosis under lipotoxic conditions, while SAD-A overexpression inhibits apoptosis; SAD-A silencing increases ER stress and inhibits autophagic flux. siRNA knockdown, overexpression, Western blotting for pBad-S155, apoptosis assays, ER stress markers, autophagic flux assay Biochemical and biophysical research communications Medium 30573363
2019 On C57BL/6N background, SAD-A (BRSK2) is essential for cortical neuronal migration and differentiation; Sada-/- mice show disorganized cortical lamination, delayed radial migration confirmed by BrdU birthdating and in utero electroporation/time-lapse imaging; SAD-A deficiency shortens axon length in hippocampal neurons in culture. Knockout mice (C57BL/6N), BrdU birthdating, in utero electroporation with pCAG-EGFP, time-lapse imaging, hippocampal neuron culture with morphometric analysis Cerebral cortex High 30307479
2020 BRSK2 kinase activity suppresses NRF2-dependent transcription and NRF2 protein levels; BRSK2 drives AMPK signaling and suppresses mTOR pathway, leading to reduced ribosome-RNA complexes, inhibited global protein synthesis, and lowered NRF2 protein levels. Gain-of-function kinase screen, integrated phosphoproteomics, RNAseq, NRF2 reporter assays, kinase-dead mutant controls Journal of cell science Medium 32546533
2020 GW296115 is a potent cell-active inhibitor of BRSK2 (IC50 <100 nM) that directly engages BRSK2 and downregulates BRSK2-driven phosphorylation and downstream signaling. KINOMEscan enzymatic profiling (403 kinases), cellular thermal shift assay (target engagement), downstream phosphorylation western blotting Scientific reports Medium 32985588
2023 BRSK2 protein levels are elevated in β-cells from T2DM patients and HFD-fed mice due to enhanced protein stability; BRSK2 senses lipid signals and induces basal insulin secretion in a kinase-dependent manner; β-cell-specific Brsk2 knockout mice are protected from HFD-induced hyperinsulinemia and insulin resistance. Inducible β-cell-specific knockout mice, gain-of-function BRSK2 mouse model, HFD feeding, kinase-dead mutant, insulin secretion assays Journal of molecular cell biology High 37188647
2024 BRSK2 mediates phosphorylation of PIMREG at Ser16, which promotes PIMREG ubiquitination-dependent degradation; loss of BRSK2 (via miR-3960 targeting) stabilizes PIMREG, activates NF-κB signaling, and promotes cisplatin resistance in triple-negative breast cancer cells. miRNA overexpression, BRSK2 knockdown/rescue, phosphorylation assays (Ser16-PIMREG), ubiquitination assay, NF-κB reporter, cisplatin resistance assays Cancer letters Medium 38582395
2025 Endogenous BRSK2 associates with the Vps34-class III PI3K-Beclin-1-ATG14 autophagy signaling complexes; BRSK2 regulates basal autophagy and activates AKT, STAT3, and NF-κB-mediated cancer cell survival; inhibition of BRSK2 by siRNA or GW296115 reduces nutrient-deprivation-induced autophagy and metastatic potential. Co-immunoprecipitation of BRSK2 with autophagy complex components, siRNA knockdown, kinase inhibitor (GW296115), autophagy flux assays, cell survival/metastasis assays Scientific reports Medium 41258112

Source papers

Stage 0 corpus · 35 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 SAD: a presynaptic kinase associated with synaptic vesicles and the active zone cytomatrix that regulates neurotransmitter release. Neuron 96 16630837
1990 Heterogeneity of Drosophila nicotinic acetylcholine receptors: SAD, a novel developmentally regulated alpha-subunit. The EMBO journal 75 1697262
2003 SAD: a new DOF protein from barley that activates transcription of a cathepsin B-like thiol protease gene in the aleurone of germinating seeds. The Plant journal : for cell and molecular biology 73 12535346
2008 C-terminal phosphorylation of LKB1 is not required for regulation of AMP-activated protein kinase, BRSK1, BRSK2, or cell cycle arrest. The Journal of biological chemistry 52 18854318
2012 Brain-selective kinase 2 (BRSK2) phosphorylation on PCTAIRE1 negatively regulates glucose-stimulated insulin secretion in pancreatic β-cells. The Journal of biological chemistry 40 22798068
2012 Synapses of amphids defective (SAD-A) kinase promotes glucose-stimulated insulin secretion through activation of p21-activated kinase (PAK1) in pancreatic β-Cells. The Journal of biological chemistry 39 22669945
2013 SAD-A kinase controls islet β-cell size and function as a mediator of mTORC1 signaling. Proceedings of the National Academy of Sciences of the United States of America 37 23922392
2016 Epigenetic Variability across Human Populations: A Focus on DNA Methylation Profiles of the KRTCAP3, MAD1L1 and BRSK2 Genes. Genome biology and evolution 30 27503294
2017 BRSK2 induced by nutrient deprivation promotes Akt activity in pancreatic cancer via downregulation of mTOR activity. Oncotarget 25 28591720
2020 Gain-of-function genetic screen of the kinome reveals BRSK2 as an inhibitor of the NRF2 transcription factor. Journal of cell science 24 32546533
2019 Deleterious Variation in BRSK2 Associates with a Neurodevelopmental Disorder. American journal of human genetics 20 30879638
2012 BRSK2 is regulated by ER stress in protein level and involved in ER stress-induced apoptosis. Biochemical and biophysical research communications 19 22713462
2013 SAD-A potentiates glucose-stimulated insulin secretion as a mediator of glucagon-like peptide 1 response in pancreatic β cells. Molecular and cellular biology 18 23629625
2024 SOD1-high fibroblasts derived exosomal miR-3960 promotes cisplatin resistance in triple-negative breast cancer by suppressing BRSK2-mediated phosphorylation of PIMREG. Cancer letters 17 38582395
2020 PKIS deep dive yields a chemical starting point for dark kinases and a cell active BRSK2 inhibitor. Scientific reports 14 32985588
2019 Isozyme-Specific Role of SAD-A in Neuronal Migration During Development of Cerebral Cortex. Cerebral cortex (New York, N.Y. : 1991) 14 30307479
2006 BRSK2 is activated by cyclic AMP-dependent protein kinase A through phosphorylation at Thr260. Biochemical and biophysical research communications 14 16870137
2012 APC/C(Cdh1) targets brain-specific kinase 2 (BRSK2) for degradation via the ubiquitin-proteasome pathway. PloS one 12 23029325
2012 Jab1 interacts with brain-specific kinase 2 (BRSK2) and promotes its degradation in the ubiquitin-proteasome pathway. Biochemical and biophysical research communications 10 22609399
2013 SAD-A and AMPK kinases: the "yin and yang" regulators of mTORC1 signaling in pancreatic β cells. Cell cycle (Georgetown, Tex.) 9 24047693
2023 BRSK2 in pancreatic β cells promotes hyperinsulinemia-coupled insulin resistance and its genetic variants are associated with human type 2 diabetes. Journal of molecular cell biology 8 37188647
2018 SAD-A Promotes Glucose-Stimulated Insulin Secretion Through Phosphorylation and Inhibition of GDIα in Male Islet β Cells. Endocrinology 8 29873699
2025 Genetic variation reveals the therapeutic potential of BRSK2 in idiopathic pulmonary fibrosis. BMC medicine 5 39838395
2018 SAD-A, a downstream mediator of GLP-1 signaling, promotes the phosphorylation of Bad S155 to regulate in vitro β-cell functions. Biochemical and biophysical research communications 5 30573363
2010 [Clinical implication of BRSK2 expression in pancreatic ductal adenocarcinoma]. Zhonghua yi xue za zhi 5 20646422
2013 BRSK2 is a valosin-containing protein (VCP)-interacting protein that affects VCP functioning in endoplasmic reticulum-associated degradation. Biotechnology letters 4 23907667
2023 Denitrification effect and strengthening mechanism of SAD/A system at low temperature by gel-immobilization technology. The Science of the total environment 3 37516176
2023 Case report: A novel frameshift mutation in BRSK2 causes autism in a 16-year old Chinese boy. Frontiers in psychiatry 3 37671287
2023 Dynamic Regulation of brsk2 in the Social and Motor Development of Zebrafish: A Developmental Behavior Analysis. International journal of molecular sciences 3 38003696
2023 Whole genome analysis of rare deleterious variants adds further evidence to BRSK2 and other risk genes in Autism Spectrum Disorder. Research square 2 37961520
2025 BRSK2 plays a role in autophagy and cancer cell growth and survival under nutrient deprivation stress via the PIK3C3 pathway. Scientific reports 1 41258112
2026 Catatonia and regression in an autism spectrum disorder patient harbouring a BRSK2 frameshift mutation. Journal of medical genetics 0 41423339
2026 Role and Impact of the brsk2 Gene in Zebrafish Retinal Development and Visual Function Characterized by Behavioral, Histological, and Transcriptomic Analyses. International journal of molecular sciences 0 41596506
2026 Advanced nitrogen removal from secondary effluent using the SAD/A process under the toxicity of PFOA. Journal of hazardous materials 0 41985285
2025 A directionally evolved genomic feature in BRSK2 harbors divergent alleles in neurocognitive disorders. Scientific reports 0 40594678

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