Affinage

VTI1A

Vesicle transport through interaction with t-SNAREs homolog 1A · UniProt Q96AJ9

Length
217 aa
Mass
25.2 kDa
Annotated
2026-06-11
23 papers in source corpus 15 papers cited in narrative 15 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

VTI1A is a Qb-SNARE protein of the trans-Golgi network and endosomal membranes that organizes vesicle biogenesis and cargo sorting by assembling into multiple distinct SNARE complexes, supporting both constitutive secretory traffic and regulated exocytosis (PMID:9705316, PMID:30143604). At the Golgi it binds alpha-SNAP and co-immunoprecipitates with syntaxin 5 and syntaxin 6, defining at least two Golgi SNARE complexes, and functional antibody microinjection arrests VSV-G secretory transport, establishing a direct role in the secretory pathway (PMID:9705316). Loss of VTI1A (together with its paralog VTI1B) impairs efficient exit of secretory cargo and secretory machinery — including SNAP-25 and dense-core vesicle cargo — from the Golgi, reducing synaptic SNAP-25 levels, disrupting retrograde cholera toxin trafficking, and yielding fewer, smaller dense-core vesicles; rescue requires long-term re-expression, placing VTI1A function in an upstream vesicle-generation step rather than the final fusion reaction (PMID:24902738, PMID:30143604). VTI1A and VTI1B act redundantly in this role, and their combined loss causes perinatal lethality with massive neurodegeneration, cortical layer 5 disorganization, and abolished neurotrophin- and enlargeosome-stimulated neurite outgrowth, the latter mediated by a complex of VTI1A/B with VAMP-4, syntaxin 16, and syntaxin 6 (PMID:21262811, PMID:33774122, PMID:36419086). A brain-specific splice variant, Vti1a-beta, resides on synaptic vesicles, co-purifies with synaptobrevin, and selectively maintains high-frequency spontaneous neurotransmitter release through a pool that recycles under resting conditions; this activity is held in check by autoinhibition and by direct binding of the synaptotagmin-11 C2A domain to VTI1A (PMID:10908612, PMID:22243751, PMID:34599505). Beyond its trafficking roles, a VTI1A-TCF7L2 (TCF4) gene fusion in colorectal cancer drives anchorage-independent growth and acts as a dominant-negative regulator of Wnt signaling (PMID:21892161, PMID:29975781).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1998 High

    Establishing whether VTI1A is a functional SNARE answered how a newly identified Golgi membrane protein participates in secretory traffic, defining it as a component of multiple Golgi SNARE complexes essential for transport.

    Evidence GST-alpha-SNAP pulldown, Co-IP with syntaxin 5/6, and antibody microinjection blocking VSV-G transport from Golgi extracts

    PMID:9705316

    Open questions at the time
    • Did not resolve which complex serves which cargo step
    • No structural model of the SNARE complexes
    • Endosomal versus Golgi partitioning not delineated
  2. 2000 High

    Identifying a brain-specific splice variant on synaptic vesicles distinguished a neuronal recycling/biogenesis pool of VTI1A from its exocytic Golgi role.

    Evidence Subcellular fractionation, synaptic vesicle immunoisolation, and Co-IP showing co-purification with synaptobrevin but not syntaxin 1/SNAP-25

    PMID:10908612

    Open questions at the time
    • Functional consequence of the 7-aa insertion not tested in vivo
    • Composition of the Vti1a-beta SNARE complex incomplete
    • Did not establish role in release versus recycling
  3. 2005 Medium

    Finding VTI1A on GLUT4 vesicles extended its trafficking role to insulin-regulated secretion in adipocytes, identifying a shared step for GLUT4 and adiponectin.

    Evidence Mass spectrometry of purified GLUT4 vesicles plus siRNA knockdown with glucose uptake and Acrp30 secretion readouts in 3T3-L1 cells

    PMID:16131485

    Open questions at the time
    • SNARE complex partners on GLUT4 vesicles not defined
    • Direct versus indirect role in glucose uptake unresolved
    • Single cell-line system
  4. 2009 Medium

    Demonstrating a VAMP7/VTI1A route for Kv4/KChIP1 channels showed VTI1A mediates a non-conventional, cargo-selective trafficking pathway to the cell surface.

    Evidence siRNA knockdown of Vti1a or VAMP7 with surface-trafficking readouts and parallel negative controls (VSVG, KChIP2) in HeLa and Neuro2A

    PMID:19138172

    Open questions at the time
    • Full SNARE complex composition not biochemically reconstituted
    • Mechanism of cargo selectivity unknown
    • Single lab
  5. 2011 High

    Comparing single versus double vti1a/vti1b knockouts established genetic redundancy and revealed a neuron-specific essentiality, since only neurons cannot substitute other SNAREs.

    Evidence Single and double null mice with histology and fibroblast viability/trafficking assays

    PMID:21262811

    Open questions at the time
    • Molecular basis of neuronal non-redundancy not defined
    • Which trafficking step causes neurodegeneration unresolved
    • Compensating SNAREs in fibroblasts not identified
  6. 2011 Medium

    Discovery of a recurrent VTI1A-TCF7L2 fusion in colorectal cancer linked the locus to oncogenic dependency independent of its SNARE function.

    Evidence Whole-genome sequencing of colorectal tumors and RNAi knockdown with anchorage-independent growth assay in NCI-H508

    PMID:21892161

    Open questions at the time
    • Mechanism of growth dependency not defined at the time
    • Fusion frequency low (3/97)
    • Contribution of VTI1A portion unclear
  7. 2012 High

    Live imaging plus electrophysiology defined a resting-recycling synaptic vesicle pool marked by VTI1A that selectively sustains spontaneous release, and truncation analysis revealed autoinhibition.

    Evidence Multicolor live imaging at single synapses, dominant-negative truncation, and mEPSC/mIPSC recordings

    PMID:22243751

    Open questions at the time
    • Molecular basis of autoinhibition not identified
    • How VTI1A distinguishes spontaneous from evoked pools unknown
    • SNARE partners for spontaneous release not specified
  8. 2014 High

    Re-expression timing in null chromaffin cells placed VTI1A function at an upstream dense-core vesicle biogenesis step rather than the final Ca2+-triggered fusion event.

    Evidence Null mouse chromaffin cells with amperometry, Ca2+ imaging, EM, and long- versus short-term rescue

    PMID:24902738

    Open questions at the time
    • Identity of the biogenesis-step SNARE complex unresolved
    • Why vti1b cannot compensate here unexplained
    • Link between DCV size and synaptobrevin loading not mechanistic
  9. 2018 High

    Double-null neuron studies unified the secretory phenotype into a Golgi cargo-sorting mechanism, showing VTI1A/B sort both secretion machinery (SNAP-25) and DCV cargo for efficient Golgi exit.

    Evidence Vti1a/b double KO neurons with live cargo imaging, EM, electrophysiology, and rescue by either paralog

    PMID:30143604

    Open questions at the time
    • Cargo recognition/sorting determinants not identified
    • Distinction between TGN sorting and earlier Golgi steps incomplete
    • Mechanism of retrograde cholera toxin defect unresolved
  10. 2018 Medium

    Functional analysis of the cancer fusion showed VTI1A-TCF4 acts as a dominant-negative Wnt regulator and that the VTI1A promoter is driven by CDX2, clarifying the fusion's signaling consequence.

    Evidence Wnt luciferase reporter assays, overexpression in colon cancer lines, and promoter/CDX2 transcription assays

    PMID:29975781

    Open questions at the time
    • How dominant-negative Wnt activity promotes growth is paradoxical and unexplained
    • In vivo relevance not tested
    • Single-lab reporter readouts
  11. 2021 High

    Identifying synaptotagmin-11 as a direct VTI1A partner provided the molecular brake on spontaneous release, with genetic epistasis placing VTI1A downstream of Syt11 inhibition.

    Evidence GST pulldown, Co-IP, affinity purification, C2A domain mapping, and vti1a knockdown rescuing Syt11 KO release in electrophysiology

    PMID:34599505

    Open questions at the time
    • Structural basis of C2A-VTI1A binding unresolved
    • Whether this interaction underlies the earlier autoinhibition not connected
    • Regulation of the interaction in vivo unknown
  12. 2021 Medium

    Cortical development studies showed VTI1A/B are required for neural progenitor maintenance and survival of layer 5 projection neurons, extending the trafficking role to developmental neurogenesis.

    Evidence Vti1a/b double null mouse with histology, immunofluorescence, and apoptosis assays

    PMID:33774122

    Open questions at the time
    • Cell-autonomous versus non-autonomous mechanism unclear
    • Specific cargo whose mistrafficking causes L5 loss not identified
    • Single lab
  13. 2022 Medium

    Defining the SNARE complex for induced neurite outgrowth (VTI1A/B Qb with VAMP-4, syntaxin 16, syntaxin 6) and the loss of dendritic Golgi outposts connected VTI1A trafficking to neuronal morphogenesis.

    Evidence Double KO hippocampal/cortical neurons with Golgi outpost imaging, neurite measurement, and neurotrophic factor/Y27632 stimulation

    PMID:36419086

    Open questions at the time
    • Complex composition inferred genetically, not reconstituted
    • How outpost loss limits neurite elongation mechanistically unclear
    • Cargo delivered by this complex not defined
  14. 2022 Medium

    Detailed Golgi marker analysis showed VTI1A/B maintain TGN recycling-protein distribution and cis-/medial Golgi organization through a mechanism only partly attributable to sphingolipid homeostasis.

    Evidence Double KO neurons with multiple Golgi markers, retrograde cholera toxin assay, and sphingolipid pathway perturbation/rescue attempts

    PMID:36460703

    Open questions at the time
    • Sphingolipid-independent mechanism not identified
    • Causal link between marker mislocalization and secretion defect incomplete
    • Single lab
  15. 2024 Medium

    A neuroblastoma double-knockout model placed VTI1A/B upstream of BDNF/Erk and enlargeosome/Akt growth-factor signaling during differentiation and neurite outgrowth.

    Evidence CRISPR/Cas9 double KO N1E-115 cells with neurite measurement, Akt/Erk phosphorylation blots, and neurotrophic factor/Y27632 stimulation

    PMID:39406055

    Open questions at the time
    • How a trafficking SNARE controls Akt/Erk signaling mechanistically unclear
    • Receptor whose trafficking is affected not identified
    • Single cell-line system

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular determinants by which VTI1A selects specific cargo at the Golgi/TGN, the structural basis of its autoinhibition and synaptotagmin-11 binding, and how its trafficking loss feeds into growth-factor signaling cascades remain unresolved.
  • No structure of VTI1A SNARE complexes or the Syt11 interaction
  • Cargo-sorting recognition code at the TGN undefined
  • Mechanistic link between SNARE function and Akt/Erk/Wnt signaling unestablished

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005794 Golgi apparatus 4 GO:0031410 cytoplasmic vesicle 3 GO:0005768 endosome 1
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-1266738 Developmental Biology 3 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-9609507 Protein localization 2
Partners
NAPASTX16STX5STX6SYT11VAMP4VAMP7VTI1B
Complex memberships
Golgi SNARE complex (syntaxin 5/syntaxin 6)VAMP-4/syntaxin 16/syntaxin 6 SNARE complexVAMP7/Vti1a SNARE complexsynaptic vesicle SNARE complex (with synaptobrevin)

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 VTI1A (Vti1-rp2) is a 29-kDa integral membrane SNARE protein enriched in the Golgi membrane. It binds alpha-SNAP (retained on GST-alpha-SNAP affinity resin from Golgi extracts), co-immunoprecipitates with syntaxin 5 and syntaxin 6, indicating participation in at least two distinct Golgi SNARE complexes. Antibody microinjection against Vti1-rp2 arrested VSV-G protein transport at the Golgi, establishing a functional role in the secretory pathway. Subcellular fractionation, indirect immunofluorescence, GST-alpha-SNAP pulldown, co-immunoprecipitation, antibody microinjection with VSV-G trafficking assay The Journal of biological chemistry High 9705316
2000 A brain-specific splice variant, Vti1a-beta (with a 7-amino-acid insertion near the SNARE-interacting helix), is enriched in small synaptic vesicles and clathrin-coated vesicles from nerve terminals. It co-purifies with synaptobrevin during immunoisolation of synaptic vesicles and forms a distinct SNARE complex that binds NSF and alpha-SNAP but does not co-immunoprecipitate with syntaxin 1 or SNAP-25, indicating it functions in a recycling/biogenesis step rather than exocytosis. Subcellular fractionation, immunoisolation of synaptic vesicles, co-immunoprecipitation, SDS-PAGE/immunoblot The Journal of neuroscience High 10908612
2005 Vti1a is a component of insulin-sensitive GLUT4-containing vesicles in 3T3-L1 adipocytes (identified by mass spectrometry in purified GLUT4 membranes). Insulin treatment depletes Vti1a from these membranes. siRNA-mediated knockdown of Vti1a significantly inhibited both adiponectin (Acrp30) secretion and insulin-stimulated glucose uptake, establishing Vti1a as a regulator of a common trafficking step for GLUT4 and Acrp30. Proteomics/mass spectrometry of purified vesicles, siRNA knockdown, deoxyglucose uptake assay, secretion assay, immunofluorescence colocalization The Journal of biological chemistry Medium 16131485
2009 Vti1a co-localizes with VAMP7 on KChIP1-expressing intracellular vesicles in HeLa and Neuro2A cells. siRNA knockdown of either Vti1a or VAMP7 inhibited Kv4/KChIP1 traffic to the plasma membrane but had no effect on conventional VSVG traffic or KChIP2-stimulated Kv4.2 traffic, defining a VAMP7/Vti1a-containing SNARE complex that mediates a non-conventional trafficking route to the cell surface. siRNA knockdown, immunofluorescence colocalization, cell-surface trafficking assay The Biochemical journal Medium 19138172
2011 Double knockout of vti1a and vti1b in mice results in perinatal lethality with major axon tract defects and >95% neuron loss in dorsal root and geniculate ganglia at E18.5, while single knockouts are viable without these defects. Fibroblasts lacking both SNAREs survive with intact organelle morphology and minor trafficking defects, indicating that more distantly related SNAREs can substitute in endosomal traffic in non-neuronal cells but not in neurons. Genetic knockout (double and single null mice), histology, immunofluorescence, cell viability assays in fibroblasts Proceedings of the National Academy of Sciences of the United States of America High 21262811
2011 A VTI1A-TCF7L2 in-frame gene fusion is found in 3/97 colorectal cancers. The fusion protein lacks the TCF4 β-catenin-binding domain. The colorectal carcinoma cell line NCI-H508 harboring the fusion is dependent on VTI1A-TCF7L2 for anchorage-independent growth, as demonstrated by RNAi-mediated knockdown. Whole-genome sequencing, RNAi knockdown, anchorage-independent growth assay Nature genetics Medium 21892161
2012 Vti1a marks a synaptic vesicle pool that recycles preferentially under resting conditions and selectively maintains high-frequency spontaneous neurotransmitter release. Loss of vti1a function specifically reduced spontaneous miniature release detected postsynaptically. Expression of a truncated vti1a augmented spontaneous release more than full-length vti1a, indicating an autoinhibitory mechanism regulates vti1a function. Multicolor live imaging at individual synapses, loss-of-function (dominant-negative truncation), electrophysiological recordings (mEPSC/mIPSC frequency) Neuron High 22243751
2014 Vti1a is absent from mature dense-core vesicles (DCVs) in adrenal chromaffin cells but localizes near the trans-Golgi network (partially overlapping with syntaxin-6). Vti1a null cells have fewer and smaller DCVs with reduced synaptobrevin-2 content and fewer Ca2+-channels at the plasma membrane, impairing exocytosis. Release kinetics and Ca2+-sensitivity are unchanged. Long-term (days) but not short-term (hours) re-expression restores secretion, placing vti1a function in an upstream vesicle biogenesis/generation step rather than in the final fusion reaction. Additional deletion of vti1b did not exacerbate the phenotype; vti1b null cells showed no secretion defects. Immunofluorescence/localization, null mouse chromaffin cells, carbon-fiber amperometry, Ca2+ imaging, electron microscopy, rescue by long-term vs. short-term re-expression The EMBO journal High 24902738
2018 Vti1a/b-deficient neurons show severely impaired synaptic vesicle and dense-core vesicle secretion. Synaptic levels of SNAP-25 are reduced to ~50%, and both SNAP-25 and DCV cargo accumulate in the Golgi. Cargo exits the Golgi less efficiently but enters normally. Retrograde cholera toxin trafficking is compromised while Sortilin/Sorcs1 distribution is unaffected. Either Vti1a or Vti1b expression alone rescues these defects. Distended Golgi cisternae and vacuoles are observed. Conclusion: Vti1a/b support regulated secretion by sorting secretory cargo and secretion machinery at the Golgi. Vti1a/b double KO neurons, live-cell imaging of cargo trafficking, immunofluorescence, electrophysiology (SV secretion), electron microscopy Nature communications High 30143604
2018 The VTI1A-TCF4 fusion protein acts as a dominant-negative regulator of Wnt signaling: NCI-H508 cells carrying the fusion show no active Wnt signaling, and overexpression of the fusion in LS174T cells inhibits a Wnt signaling luciferase reporter. The VTI1A promoter is highly active in colon cancer cells and is transcriptionally activated by the intestinal homeodomain factor CDX2. Luciferase reporter assay (Wnt signaling), overexpression in colon cancer cell lines, promoter-reporter assay, CDX2 transcription factor assay PloS one Medium 29975781
2021 Synaptotagmin-11 (Syt11) directly interacts with vti1a and suppresses spontaneous neurotransmission through it. GST pulldown, co-immunoprecipitation, and affinity purification demonstrated direct Syt11–vti1a interaction. The C2A domain of Syt11 binds vti1a with high affinity. Knockdown of vti1a reversed the elevated spontaneous release phenotype of Syt11 knockout neurons, placing vti1a downstream of Syt11 inhibition. GST pulldown, co-immunoprecipitation, affinity purification, domain deletion analysis, siRNA knockdown of vti1a in Syt11 KO neurons, electrophysiology (mEPSC frequency) Journal of neurochemistry High 34599505
2021 Vti1a and Vti1b are required for cortical development: their double null mutation depletes neural progenitor pools and causes distinctive disorganization of cortical layer 5, with apoptosis of Ctip2-expressing L5 neurons and loss of corticospinal and callosal projections. Vti1a/b double null mouse, histology, immunofluorescence, apoptosis assays Neuroscience Medium 33774122
2022 In the absence of vti1a and vti1b, hippocampal neurons lack Golgi outposts in dendrites and cortical neurons have significantly shorter neurites. Neurite elongation stimulated by neurotrophic factors (NGF, BDNF, NT-3, GDNF) or ROCK inhibitor Y27632 (enlargeosome exocytosis) is abolished in double-deficient neurons. vti1a or vti1b functions as the Qb-SNARE in a complex with VAMP-4 (R-SNARE), syntaxin 16 (Qa-SNARE), and syntaxin 6 (Qc-SNARE) required for induced neurite outgrowth. Double KO primary neurons (hippocampal and cortical), immunofluorescence for Golgi outposts, neurite length measurement, neurotrophic factor/Y27632 stimulation, Western blotting of postsynaptic densities Neural development Medium 36419086
2022 In Vti1a/b-deficient neurons, the cis-/medial Golgi (GM130, giantin staining) is increased while TGN recycling proteins TGN38 and TMEM87A are decreased, without overall reduction in Golgi size or absence of TGN compartment. DCV cargo markers and LAMP1/KDEL distribution are altered. Cholera Toxin retrograde trafficking is disrupted. Partial phenocopy is achieved by disturbing sphingolipid homeostasis, but overexpression of sphingomyelin synthases or myriocin treatment does not rescue, indicating that Vti1a/b are required for distinct aspects of TGN and cis-/medial Golgi organization beyond sphingolipid regulation. Vti1a/b double KO neurons, immunofluorescence for Golgi markers, live retrograde trafficking assay (Cholera Toxin), sphingolipid pathway perturbation Scientific reports Medium 36460703
2024 CRISPR/Cas9-generated Vti1a/Vti1b double knockout in N1E-115 neuroblastoma cells impairs differentiation, reduces synaptic protein levels, and reduces neurite formation and elongation. Y27632 (enlargeosome exocytosis via Rho kinase inhibition) fails to stimulate neurite elongation in DKO cells, and Akt signaling during enlargeosome-mediated outgrowth is disrupted. BDNF-induced neurite outgrowth is also impaired, with disrupted Erk signaling, placing vti1a/b upstream of these growth factor signaling cascades. CRISPR/Cas9 double KO, neurite length measurement, Western blotting (Akt, Erk phosphorylation), neurotrophic factor stimulation assays European journal of cell biology Medium 39406055

Source papers

Stage 0 corpus · 23 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Genomic sequencing of colorectal adenocarcinomas identifies a recurrent VTI1A-TCF7L2 fusion. Nature genetics 246 21892161
2012 Vti1a identifies a vesicle pool that preferentially recycles at rest and maintains spontaneous neurotransmission. Neuron 143 22243751
2000 The SNARE Vti1a-beta is localized to small synaptic vesicles and participates in a novel SNARE complex. The Journal of neuroscience : the official journal of the Society for Neuroscience 80 10908612
2011 Lack of the endosomal SNAREs vti1a and vti1b led to significant impairments in neuronal development. Proceedings of the National Academy of Sciences of the United States of America 55 21262811
1998 A 29-kilodalton Golgi soluble N-ethylmaleimide-sensitive factor attachment protein receptor (Vti1-rp2) implicated in protein trafficking in the secretory pathway. The Journal of biological chemistry 54 9705316
2018 Vti1a/b regulate synaptic vesicle and dense core vesicle secretion via protein sorting at the Golgi. Nature communications 47 30143604
2005 The v-SNARE Vti1a regulates insulin-stimulated glucose transport and Acrp30 secretion in 3T3-L1 adipocytes. The Journal of biological chemistry 43 16131485
2009 A VAMP7/Vti1a SNARE complex distinguishes a non-conventional traffic route to the cell surface used by KChIP1 and Kv4 potassium channels. The Biochemical journal 41 19138172
2014 The SNARE protein vti1a functions in dense-core vesicle biogenesis. The EMBO journal 37 24902738
2017 Cumulative evidence for relationships between multiple variants in the VTI1A and TCF7L2 genes and cancer incidence. International journal of cancer 18 28949031
2020 Vesicle transport through interaction with t-SNAREs 1a (Vti1a)'s roles in neurons. Heliyon 14 32775753
2018 The VTI1A-TCF4 colon cancer fusion protein is a dominant negative regulator of Wnt signaling and is transcriptionally regulated by intestinal homeodomain factor CDX2. PloS one 13 29975781
2022 Primary neurons lacking the SNAREs vti1a and vti1b show altered neuronal development. Neural development 11 36419086
2021 Synaptotagmin-11 inhibits spontaneous neurotransmission through vti1a. Journal of neurochemistry 11 34599505
2022 The Role of Vti1a in Biological Functions and Its Possible Role in Nervous System Disorders. Frontiers in molecular neuroscience 9 35711736
2022 Epigenome-Wide Association Study Identified VTI1A DNA Methylation Associated With Accelerometer-Assessed Physical Activity. Medicine and science in sports and exercise 8 35700439
2021 Ablation of Vti1a/1b Triggers Neural Progenitor Pool Depletion and Cortical Layer 5 Malformation in Late-embryonic Mouse Cortex. Neuroscience 8 33774122
2015 Single nucleotide polymorphisms in VTI1A gene contribute to the susceptibility of Chinese population to non-small cell lung cancer. The International journal of biological markers 7 25744365
2022 Vti1a/b support distinct aspects of TGN and cis-/medial Golgi organization. Scientific reports 4 36460703
2019 Detection of Novel Fusion Transcript VTI1A-CFAP46 in Hepatocellular Carcinoma. Gastrointestinal tumors 4 31602373
2024 The double deficiency of the SNARE proteins vti1a and vti1b affects neurite outgrowth and signaling in N1E-115 neuroblastoma cells. European journal of cell biology 2 39406055
2026 Alterations in bone malformation in the absence of the endosomal SNAREs Vti1a and Vti1b. PloS one 0 41838692
2026 Reduction in Synaptic Vesicle Protein Abundance but Increased Amounts of Nsg2 and Lpcat1 in Cerebral Cortices Without the Endosomal SNARE Proteins Vti1a and Vti1b. Proteomics 0 41859820

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