Affinage

GOLGB1

Golgin subfamily B member 1 · UniProt Q14789

Length
3259 aa
Mass
376.0 kDa
Annotated
2026-06-10
32 papers in source corpus 22 papers cited in narrative 22 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

Giantin (GOLGB1) is a large integral Golgi membrane protein with an extended coiled-coil cytoplasmic domain, a C-terminal transmembrane anchor, and a disulfide-linked luminal domain, positioned to form intercisternal cross-bridges of the Golgi complex (PMID:7691276, PMID:7511208). In the classical vesicle-tethering model, giantin resides on COPI vesicles and serves as the vesicle-side receptor for p115, which bridges to GM130 on the cis-Golgi membrane; its N-terminal ~15% is sufficient for p115 binding and acts as a long flexible tether linking vesicles to cisternae (PMID:9490716, PMID:10644749), with giantin functioning at a step in ER-to-Golgi transport downstream of GM130 (PMID:11035033). Giantin localizes through its C-terminal cytoplasmic domain, which recruits the peripheral protein GCP60, and it engages the small GTPases Rab1 and Rab6A (PMID:11590181, PMID:17475246). Beyond tethering, giantin organizes the Golgi ribbon — it is necessary and sufficient to cluster Golgi stacks (PMID:23555793) — and its luminal disulfide-mediated dimerization state governs post-stress Golgi reassembly, with Rab6a-assisted re-dimerization required to re-recruit a subset of giantin-dependent resident enzymes via direct binding of their cytoplasmic tails to the giantin N-terminus (PMID:30453527, PMID:31847122). A central function is the control of glycosylation and sulfation: giantin governs the Golgi localization and expression of specific glycosyltransferases and sulfotransferases, including GALNT3 and the Gal3-O-sulfotransferases, such that its loss redistributes enzyme targeting to a GM130-GRASP65 route and alters N-glycan and mucin sulfation (PMID:29093022, PMID:28782625, PMID:39388276). Through these activities giantin is required for tissue morphogenesis and secretory cargo maturation: loss-of-function abolishes giantin expression and causes osteochondrodysplasia, dwarfism and cleft palate in rat and mouse models with defective glycosylation (PMID:21851869, PMID:27226319), disrupts coordinated chondrocyte ECM secretion (PMID:29577904), impairs intracellular N-terminal procollagen propeptide processing leading to collagen mineralization defects and fractures (PMID:33944912), and supports ciliogenesis by controlling dynein-2 (WDR34) localization for retrograde intraflagellar transport (PMID:24046448, PMID:28546340).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1993 High

    Established giantin's membrane topology — an integral Golgi protein with a massive cytoplasmic domain and disulfide-linked luminal domain — providing the structural basis for a cross-bridging role.

    Evidence Limited proteolysis, carbonate extraction, non-reducing SDS-PAGE and immunofluorescence on isolated Golgi vesicles

    PMID:7691276

    Open questions at the time
    • Cross-bridging function inferred from topology, not demonstrated functionally
    • No binding partners identified at this stage
  2. 1994 High

    Molecular cloning revealed an extraordinarily coiled-coil-rich 376 kDa protein, defining giantin as an extended rod-like golgin.

    Evidence cDNA cloning, heptad-repeat sequence analysis, immunoelectron microscopy

    PMID:7511208

    Open questions at the time
    • No functional partners or mechanism
    • Structural model of the coiled-coil not resolved
  3. 1998 High

    Identified giantin as a COPI-vesicle-side receptor for p115 in a p115-GM130 tethering complex, answering how vesicles dock to Golgi membranes.

    Evidence Co-IP of p115 partners, cell-free vesicle docking assay with antibody inhibition and GM130 peptide competition

    PMID:9490716

    Open questions at the time
    • Binding sites not mapped to specific domains
    • In vivo requirement not yet tested
  4. 2000 High

    Mapped the p115-binding activity to the N-terminal ~15% of giantin and placed giantin sequentially downstream of GM130 in ER-to-Golgi transport.

    Evidence Recombinant N-terminal fragment binding, cell-free reassembly inhibition, VSV-G transport assay with inhibitory peptides/antibodies

    PMID:10644749 PMID:11035033

    Open questions at the time
    • Did not establish whether giantin is essential versus redundant in vivo
  5. 2001 Medium

    Localized the Golgi-targeting signal to the C-terminal cytoplasmic domain and identified GCP60 as a C-terminal interactor, while a separate in vivo study found that depleting giantin had no detectable effect on Golgi structure — challenging an essential tethering role.

    Evidence Yeast two-hybrid, co-IP and dominant-negative overexpression (GCP60); antibody microinjection and proteasomal antigen depletion (p115/giantin loss-of-function)

    PMID:11590181 PMID:11591729

    Open questions at the time
    • Apparent dispensability conflicts with later loss-of-function phenotypes
    • GCP60 functional consequence beyond overexpression unclear
  6. 2007 Medium

    Showed giantin binds Rab6A in addition to Rab1, indicating a single golgin can engage two distinct Rab GTPases.

    Evidence Co-IP from cells and in vitro pulldown

    PMID:17475246

    Open questions at the time
    • Functional consequence of dual Rab binding not defined
    • Rab-binding region not mapped
  7. 2011 High

    Demonstrated in vivo essentiality via a truncating Golgb1 mutation that abolishes giantin and causes lethal osteochondrodysplasia, establishing a role in chondrogenesis.

    Evidence Linkage mapping, mutant allele sequencing, Western blot and growth-plate histology in ocd/ocd rats

    PMID:21851869

    Open questions at the time
    • Molecular mechanism linking giantin loss to chondrodysplasia not yet defined
    • Cell-biological defect underlying the phenotype unknown
  8. 2013 Medium

    Defined two cell-biological functions — Golgi ribbon organization and ciliogenesis through dynein-2 localization — beyond classical vesicle tethering.

    Evidence siRNA knockdown, Drosophila S2 gain-of-function, nocodazole assays, WDR34 mislocalization and cilia measurements with pathway epistasis

    PMID:23555793 PMID:24046448

    Open questions at the time
    • Mechanism by which giantin controls dynein-2 localization unknown
    • Connection between ribbon organization and glycosylation not yet established
  9. 2016 High

    Established with multiple independent alleles that giantin loss causes cleft palate via intrinsic palatal shelf defects and impaired protein glycosylation, linking giantin to glycosylation-dependent morphogenesis.

    Evidence ENU and CRISPR/Cas9 mouse alleles, explant culture, hyaluronan and glycosylation immunostaining

    PMID:27226319

    Open questions at the time
    • Which specific glycosylation enzymes are affected not yet identified
    • Mechanistic link from glycosylation defect to shelf elevation unclear
  10. 2017 High

    Connected giantin to the Golgi targeting/expression of specific glycosyltransferases — GALNT3 in particular — showing a feedback between Golgi structure and glycosylation and recapitulating GALNT3-linked disease.

    Evidence Mammalian and zebrafish knockouts, RNA-seq, disease-phenotype comparison; PLA, N-glycan MALDI-TOF MS and GM130/giantin knockdowns in prostate cancer cells

    PMID:28782625 PMID:29093022

    Open questions at the time
    • Whether expression changes are direct or compensatory not resolved
    • Structural basis for enzyme recruitment not defined
  11. 2017 Medium

    Corroborated the ciliogenesis role in vivo, with giantin loss causing elongated cilia and tip accumulation consistent with defective retrograde IFT.

    Evidence Morpholino and CRISPR knockout in zebrafish, scanning EM of cilia

    PMID:28546340

    Open questions at the time
    • Direct demonstration of dynein-2 transport defect in vivo lacking
    • Relationship to Golgi function not dissected
  12. 2018 Medium

    Defined giantin's secretory role in chondrocyte ECM production and identified luminal disulfide dimerization as a regulated, stress-responsive state required for Golgi recovery.

    Evidence ocd/ocd chondrocyte mRNA/protein discordance for aggrecan/link protein/collagen XI; PLA dimerization assay and knockdown rescue in an ethanol stress model

    PMID:29577904 PMID:30453527

    Open questions at the time
    • Trigger and enzymology of de-dimerization not defined
    • How dimerization couples to enzyme trafficking not yet shown
  13. 2019 Medium

    Detailed the dimerization-dependent enzyme recruitment pathway during reassembly and, separately, presented electron-tomography evidence that giantin may limit rather than promote cisternal connectivity, refining the tether model.

    Evidence BFA washout with PLA/AFM/3D-SIM; electron tomography and FRAP after siRNA knockdown

    PMID:31544102 PMID:31847122

    Open questions at the time
    • Tension between tethering and anti-connectivity roles unresolved
    • Single-lab mechanistic models await independent confirmation
  14. 2021 High

    Identified a trafficking-independent requirement for giantin in intracellular N-propeptide processing of type I procollagen, explaining the skeletal/mineralization phenotype.

    Evidence Human giantin-knockout cells with GFP-procollagen assays and immunoblot; zebrafish mutant fracture and mineralization analysis

    PMID:33944912

    Open questions at the time
    • Identity of the giantin-dependent processing protease not defined
    • Mechanism coupling giantin to propeptide cleavage unknown
  15. 2024 Medium

    Extended giantin's enzyme-targeting role to sulfotransferases, showing it complexes with Gal3STs and controls their localization and mucin sulfation, with relevance to Sjögren's disease.

    Evidence Co-IP, knockout/knockdown cells, immunofluorescence, MUC5B sulfation analysis in patient biopsies

    PMID:39388276

    Open questions at the time
    • Direct versus indirect basis of Gal3ST mislocalization not resolved
    • Causal role in Sjögren's pathogenesis correlational
  16. 2026 Medium

    Linked GOLGB1 to MAPK signaling control in intervertebral disc homeostasis, placing it upstream of ERK/P38 activation in nucleus pulposus cell survival.

    Evidence Knockdown with p-ERK/p-P38 immunoblotting, proliferation/apoptosis assays, mouse IDD model with MAPK-inhibitor rescue

    PMID:41547890

    Open questions at the time
    • Mechanism connecting Golgi/giantin function to MAPK activation unknown
    • Whether the effect is direct or secondary to secretory stress unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how giantin's coiled-coil architecture and dimerization state mechanistically reconcile its vesicle-tethering, ribbon-organizing, anti-connectivity, and enzyme-recruiting functions into a single structural model.
  • No high-resolution structure of full-length giantin
  • Direct molecular link between dimerization and glycosyltransferase recruitment undefined
  • Reconciliation of pro-tethering versus anti-connectivity observations missing

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0060090 molecular adaptor activity 3
Localization
GO:0005794 Golgi apparatus 3
Pathway
R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-5653656 Vesicle-mediated transport 3
Complex memberships
giantin-p115-GM130 tethering complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 Giantin is an integral Golgi membrane protein with a large cytoplasmic domain (up to 350 kDa accessible to proteolysis from intact Golgi vesicles), a disulfide-linked lumenal domain, and a C-terminal transmembrane anchor; its topology and conservation suggest a role in forming intercisternal cross-bridges of the Golgi complex. Differential centrifugation, sucrose flotation, carbonate extraction, limited proteolysis of intact Golgi vesicles, non-reducing SDS-PAGE, double immunofluorescence with galactosyltransferase marker Molecular biology of the cell High 7691276
1994 Giantin is a 376 kDa Golgi membrane protein with an extraordinarily high content of heptad repeats, consistent with coiled-coil structure similar to myosin family proteins, localized to the Golgi complex by immunoelectron microscopy. cDNA cloning, sequence analysis of heptad repeats, immunoelectron microscopy, immunofluorescence with brefeldin A treatment, subcellular fractionation Molecular and cellular biology High 7511208
1998 Giantin is present on COPI vesicles and acts as a vesicle-side receptor for p115; the giantin–p115–GM130 tethering complex docks COPI vesicles to Golgi membranes, with giantin on the vesicle, GM130 on the Golgi membrane, and p115 bridging them. Immunoprecipitation of p115 binding partners from detergent Golgi extracts, antibody inhibition of vesicle docking in cell-free assay, GM130 peptide competition, immunodepletion The Journal of cell biology High 9490716
2000 The N-terminal 15% of giantin is sufficient to bind p115 both in vitro and in vivo, and this fragment blocks cell-free Golgi reassembly, consistent with a long flexible tether linking COPI vesicles to cisternae. In vitro binding assay with recombinant N-terminal giantin fragments, co-immunoprecipitation in vivo, cell-free Golgi reassembly inhibition assay The Journal of biological chemistry High 10644749
2000 Giantin is required for ER-to-Golgi transport: giantin p115-binding domain peptides and anti-giantin antibodies inhibit VSV-G protein transport to the mannosidase II-containing Golgi compartment at a step temporally after the GM130-requiring step, indicating giantin acts sequentially downstream of GM130 in ER-Golgi trafficking. VSV-G transport assay, inhibitory peptide injection, antibody microinjection, kinetic comparison with anti-p115 and anti-GM130 reagents The Journal of biological chemistry High 11035033
2001 The Golgi localization signal of giantin resides in its C-terminal cytoplasmic domain; a novel peripheral Golgi protein GCP60 interacts with this C-terminal domain of giantin via its own C-terminal domain, and overexpression of the GCP60 C-terminal domain causes Golgi disassembly and blocks ER-to-Golgi transport. Yeast two-hybrid screening using giantin C-terminal cytoplasmic domain as bait, co-immunoprecipitation, immunofluorescence, immunoelectron microscopy, overexpression dominant-negative analysis The Journal of biological chemistry Medium 11590181
2001 In vivo, reduction of p115 below detectable levels causes COPI-dependent Golgi fragmentation; however, reducing giantin below detectable levels or inhibiting p115 binding to GM130 has no detectable effect on Golgi structure or reassembly after cell division or brefeldin A washout, demonstrating that p115's essential role in Golgi structure is independent of giantin and GM130. Antibody microinjection targeting mapped binding sites, proteasome-mediated antigen depletion, immunofluorescence for Golgi structure, COPI inhibition co-treatment The Journal of cell biology Medium 11591729
2007 Giantin interacts with the small GTPase Rab6A (in addition to previously known Rab1) both in vivo (co-immunoprecipitation) and in vitro (pulldown), suggesting that two distinct Rab GTPases can bind to the same golgin protein. Co-immunoprecipitation from cells, in vitro pulldown assay Experimental cell research Medium 17475246
2011 A 10-bp insertion in exon 13 of Golgb1 causing a frameshift and premature stop at codon 1082 (truncating the C-terminal two-thirds including the Golgi-targeting region) abolishes giantin protein expression and causes osteochondrodysplasia, systemic edema, cleft palate, and lethal dwarfism in ocd/ocd rats, establishing giantin as essential for chondrogenesis. Fine linkage mapping, sequence analysis of mutant allele, in-gel Western blotting with C-terminal epitope antibody, histology, immunohistochemistry of growth plate Bone High 21851869
2013 Giantin is required for ciliogenesis: siRNA-mediated depletion of giantin causes mis-localization of WDR34 (dynein-2 intermediate chain) and prevents primary cilia formation; partial depletion increases cilia length, consistent with giantin controlling ciliogenesis through regulation of dynein-2 localization rather than through the Rab11-Rabin8-Rab8 ciliary membrane pathway. siRNA knockdown, immunofluorescence for cilia markers and WDR34, cilia length measurement, epistasis with Rab11/Rabin8/Rab8 pathway components Journal of cell science Medium 24046448
2013 Giantin mediates the spatial organization of the Golgi ribbon: siRNA depletion of giantin results in more dispersed Golgi mini-stacks after nocodazole treatment without changing cisternal length; exogenous expression of mammalian giantin in Drosophila S2 cells (which lack a giantin homolog and have dispersed stacks) induces clustering of Golgi stacks, demonstrating that giantin is sufficient and necessary for Golgi ribbon organization. siRNA knockdown, nocodazole treatment, immunofluorescence, exogenous expression of giantin cDNA in Drosophila S2 cells, glycosylation assays PloS one Medium 23555793
2016 Golgb1 loss-of-function mutation in mice (confirmed by CRISPR/Cas9-generated alleles) causes cleft palate with intrinsic defects in palatal shelf elevation: mutant palatal mesenchyme shows increased cell density, reduced hyaluronan accumulation, and impaired protein glycosylation, demonstrating a specific role for giantin in protein glycosylation and tissue morphogenesis. ENU mutagenesis screen, genetic linkage mapping, whole-exome sequencing, CRISPR/Cas9 genome editing, maxillary explant culture, immunostaining for hyaluronan and glycosylation markers Development (Cambridge, England) High 27226319
2017 Giantin knockout leads to near-complete loss of GALNT3 function and differential expression of 22 Golgi-resident glycosyltransferases (but not glycan-processing enzymes or ER glycosylation machinery); giantin-knockout zebrafish phenocopy hyperphosphatemic familial tumoral calcinosis (caused by GALNT3 mutations), establishing a feedback loop between Golgi structure and glycosyltransferase expression. Giantin knockout in mammalian cells and zebrafish (CRISPR/Cas9), RNA-seq, phenotypic characterization (hyperostosis, ectopic calcium deposits), comparison to GALNT3 disease phenotype Journal of cell science High 29093022
2017 In androgen-independent prostate cancer cells with defective giantin, Golgi targeting of glycosyltransferases and α-mannosidase IA shifts from giantin to GM130-GRASP65; this results in acquisition of high mannose N-glycans on trans-Golgi enzymes and cell surface glycoproteins, absent in cells with functional giantin. Confocal microscopy after knockdown of GM130 or giantin, in situ proximity ligation assay, MALDI-TOF mass spectrometry of N-glycans from immunoprecipitated enzyme Biochimica et biophysica acta. General subjects Medium 28782625
2017 Giantin loss-of-function in zebrafish causes elongated cilia in the neural tube and accumulation of material at the ciliary tip, consistent with defective retrograde intraflagellar transport, corroborating a role for giantin in ciliogenesis through retrograde dynein-2-mediated transport. Morpholino knockdown, CRISPR/Cas9 knockout in zebrafish, scanning electron microscopy of cilia, cilia number and length measurements Biology open Medium 28546340
2018 Giantin is required for coordinated production of aggrecan, link protein and type XI collagen in chondrocytes at the post-transcriptional/secretory level: ocd/ocd rat chondrocytes lacking giantin show reduced aggrecan and link protein and increased type XI collagen protein levels despite normal mRNA levels, indicating giantin is required for proper secretion/trafficking of these ECM components. Immunostaining of embryonic femur cartilage from ocd/ocd and normal rats, semi-quantitative RT-PCR for ECM mRNAs, Safranin O/azan staining of epiphyseal cartilage, isolated chondrocyte cultures Biochemical and biophysical research communications Medium 29577904
2018 Giantin exists as a dimer linked by a disulfide bond in its luminal domain; ethanol-induced Golgi disorganization is associated with giantin de-dimerization, and post-ethanol Golgi recovery requires giantin re-dimerization as well as Rab6a GTPase; knockdown of giantin, Rab6a, or non-muscle myosin IIB impairs post-ethanol Golgi recovery. Proximity ligation assay for giantin dimerization state, siRNA knockdown, immunofluorescence for Golgi structure, ethanol treatment/withdrawal model in VA-13 cells and rat hepatocytes Biomolecules Medium 30453527
2019 Giantin knockdown reduces fenestrae within Golgi cisternae and increases diffusion rate of Golgi membrane proteins, indicating increased connectivity among cisternae and stacks; this suggests giantin inhibits rather than promotes tethering/fusion of nearby Golgi cisternae, contrary to the classical cis-golgin tether model. siRNA knockdown, electron tomography and 3D modeling of Golgi, FRAP measurement of Golgi membrane protein diffusion, glycosylation assays Frontiers in cell and developmental biology Medium 31544102
2019 Post-BFA stress Golgi reassembly is governed by giantin re-dimerization via its luminal disulfide bond assisted by Rab6a GTPase; giantin-sensitive Golgi resident enzymes are recruited to nascent Golgi membranes after complete recovery via direct interaction of their cytoplasmic tails with the N-terminus of giantin, whereas GM130-GRASP65-dependent enzymes arrive earlier. Brefeldin A treatment/washout model, proximity ligation assay, atomic force microscopy of giantin conformational state, 3D SIM super-resolution microscopy Cells Medium 31847122
2021 Giantin is required for intracellular N-terminal propeptide processing of type I procollagen: in human giantin-knockout cells expressing GFP-tagged procollagen, procollagen trafficking is independent of giantin but N-propeptide cleavage of pro-α1(I) is defective; giantin-mutant zebrafish accumulate spontaneous fractures and show defective mineralization of newly deposited collagen. Human giantin-knockout cell line, GFP-tagged procollagen trafficking assay, immunoblot for N-propeptide processing, zebrafish giantin mutant fracture induction and mineralization assay, procollagen reporter expression The Journal of cell biology High 33944912
2024 Giantin forms protein complexes with Gal3-O-sulfotransferases (Gal3STs) and is required for their proper Golgi localization; loss or mislocalization of giantin (as occurs in salivary glands of Sjögren's disease patients) alters Gal3ST localization, reduces Gal3ST activity, and decreases sulfation of MUC5B mucin. Co-immunoprecipitation of giantin-Gal3ST complexes, giantin knockout and knockdown cell lines, immunofluorescence localization, MUC5B sulfation analysis from patient salivary gland biopsies JCI insight Medium 39388276
2026 GOLGB1 knockdown activates the MAPK pathway (elevated p-ERK and p-P38), promotes nucleus pulposus cell degeneration and apoptosis, and inhibits proliferation; MAPK inhibitor SCH772984 rescues the degeneration phenotype, positioning GOLGB1 upstream of MAPK signaling in intervertebral disc homeostasis. Plasmid transfection (knockdown), Western blotting for p-ERK/p-P38, EdU proliferation assay, TUNEL/flow cytometry apoptosis assay, CCK8, mouse IDD model with histology/IHC, MAPK inhibitor rescue Scientific reports Medium 41547890

Source papers

Stage 0 corpus · 32 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 Giantin, a novel conserved Golgi membrane protein containing a cytoplasmic domain of at least 350 kDa. Molecular biology of the cell 374 7691276
1998 A role for giantin in docking COPI vesicles to Golgi membranes. The Journal of cell biology 256 9490716
2001 Identification and characterization of a novel Golgi protein, GCP60, that interacts with the integral membrane protein giantin. The Journal of biological chemistry 113 11590181
2000 The p115-interactive proteins GM130 and giantin participate in endoplasmic reticulum-Golgi traffic. The Journal of biological chemistry 106 11035033
2002 CASP, the alternatively spliced product of the gene encoding the CCAAT-displacement protein transcription factor, is a Golgi membrane protein related to giantin. Molecular biology of the cell 103 12429822
2001 Evidence that Golgi structure depends on a p115 activity that is independent of the vesicle tether components giantin and GM130. The Journal of cell biology 97 11591729
2013 The golgin tether giantin regulates the secretory pathway by controlling stack organization within Golgi apparatus. PloS one 68 23555793
2000 The amino-terminal domain of the golgi protein giantin interacts directly with the vesicle-tethering protein p115. The Journal of biological chemistry 55 10644749
2016 Golgb1 regulates protein glycosylation and is crucial for mammalian palate development. Development (Cambridge, England) 54 27226319
1994 Molecular genetic analyses of a 376-kilodalton Golgi complex membrane protein (giantin). Molecular and cellular biology 45 7511208
2017 Giantin-knockout models reveal a feedback loop between Golgi function and glycosyltransferase expression. Journal of cell science 44 29093022
2007 Giantin interacts with both the small GTPase Rab6 and Rab1. Experimental cell research 40 17475246
2013 A role for the Golgi matrix protein giantin in ciliogenesis through control of the localization of dynein-2. Journal of cell science 36 24046448
2011 Insertional mutation in the Golgb1 gene is associated with osteochondrodysplasia and systemic edema in the OCD rat. Bone 34 21851869
2003 Giantin is the major Golgi autoantigen in human anti-Golgi complex sera. Arthritis research & therapy 33 15059272
2017 The Golgi matrix protein giantin is required for normal cilia function in zebrafish. Biology open 29 28546340
2015 Fusion of PDGFRB to MPRIP, CPSF6, and GOLGB1 in three patients with eosinophilia-associated myeloproliferative neoplasms. Genes, chromosomes & cancer 29 26355392
2019 The Golgin Protein Giantin Regulates Interconnections Between Golgi Stacks. Frontiers in cell and developmental biology 22 31544102
2018 Giantin Is Required for Post-Alcohol Recovery of Golgi in Liver Cells. Biomolecules 21 30453527
2017 Shifted Golgi targeting of glycosyltransferases and α-mannosidase IA from giantin to GM130-GRASP65 results in formation of high mannose N-glycans in aggressive prostate cancer cells. Biochimica et biophysica acta. General subjects 20 28782625
2021 Giantin is required for intracellular N-terminal processing of type I procollagen. The Journal of cell biology 19 33944912
2018 Giantin is required for coordinated production of aggrecan, link protein and type XI collagen during chondrogenesis. Biochemical and biophysical research communications 14 29577904
2020 A Novel 65-bp Indel in the GOLGB1 Gene Is Associated with Chicken Growth and Carcass Traits. Animals : an open access journal from MDPI 10 32178328
2019 Post-ER Stress Biogenesis of Golgi Is Governed by Giantin. Cells 9 31847122
2018 Golgi Distribution of Lyn to Caveolin- and Giantin-Positive cis-Golgi Membranes and the Caveolin-Negative, TGN46-Positive trans-Golgi Network. Biological & pharmaceutical bulletin 5 29311477
2023 A combined experimental-computational approach uncovers a role for the Golgi matrix protein Giantin in breast cancer progression. PLoS computational biology 4 37068117
2022 Pedigree-based study to identify GOLGB1 as a risk gene for bipolar disorder. Translational psychiatry 4 36115840
2020 A novel low-grade nasopharyngeal adenocarcinoma characterized by a GOLGB1-BRAF fusion gene. Genes, chromosomes & cancer 3 32951290
2024 Giantin mediates Golgi localization of Gal3-O-sulfotransferases and affects salivary mucin sulfation in patients with Sjögren's disease. JCI insight 2 39388276
2018 Association between GOLGB1 tag-polymorphisms and nonsyndromic cleft palate only in the Brazilian population. Annals of human genetics 2 29430628
2023 An Electron Tomographic Analysis of Giantin-Deficient Golgi Proposes a New Function of the Golgin Protein Family. Methods in molecular biology (Clifton, N.J.) 1 36512219
2026 GOLGB1 deficiency accelerates intervertebral disc degeneration by activating the MAPK pathway. Scientific reports 0 41547890

Missed literature

Know a paper Affinage missed for GOLGB1? Flag it for the maintainers and the community.

No submissions yet.