Family Search for PF07092 (TMEM106)
April 2024: See Interactive Tools for Functional Annotation of Bacterial Genomes for advice on using these tools.
PF07092 hits 10 sequences in PaperBLAST's database above the trusted cutoff. Showing all hits. Or show only hits to curated sequences or try another family.
T106B_RAT / Q6AYA5 Transmembrane protein 106B from Rattus norvegicus (Rat) (see paper)
Aligns to 119:259 / 275 (51.3%), covers 100.0% of PF07092, 227.1 bits
- function: Involved in dendrite morphogenesis and maintenance by regulating lysosomal trafficking. May act as a molecular brake for retrograde transport of late endosomes/lysosomes, possibly via its interaction with MAP6 (PubMed:24357581). In neurons, may also play a role in the regulation of lysosomal size and responsiveness to stress (By similarity). Required for proper lysosomal acidification (By similarity).
function: In neurons, involved in the transport of late endosomes/lysosomes (PubMed:24357581). May be involved in dendrite morphogenesis and maintenance by regulating lysosomal trafficking (PubMed:24357581). May act as a molecular brake for retrograde transport of late endosomes/lysosomes, possibly via its interaction with MAP6 (PubMed:24357581). In motoneurons, may mediate the axonal transport of lysosomes and axonal sorting at the initial segment (By similarity). It remains unclear whether TMEM106B affects the transport of moving lysosomes in the anterograde or retrograde direction in neurites and whether it is particularly important in the sorting of lysosomes in axons or in dendrites (By similarity). In neurons, may also play a role in the regulation of lysosomal size and responsiveness to stress (By similarity). Required for proper lysosomal acidification (By similarity).
subunit: Can form homomers (By similarity). Interacts (via N-terminus) with MAP6 (via C-terminus) (PubMed:24357581). Interacts (via C- terminus) with the vacuolar-type ATPase subunit ATP6AP1 (By similarity). Interacts (via N-terminus) with AP2M1 and CLTC (By similarity). Interacts with TMEM106C (By similarity). - Proteome Analysis of Urinary Biomarkers in a Bovine IRBP-Induced Uveitis Rat Model via Data-Independent Acquisition and Parallel Reaction Monitoring Proteomics
Qin, Frontiers in molecular biosciences 2022 - “...P04785 Protein disulfide-isomerase 1.53 Q793F9 Vacuolar protein sorting-associated protein 4A 1.53 P53369 7,8-dihydro-8-oxoguanine triphosphatase 1.53 Q6AYA5 Transmembrane protein 106B 1.51 P07171 Calbindin 0.62 Q4FZU2 Keratin, type II cytoskeletal 6A 0.59 P10760 Adenosylhomocysteinase 0.56 The overlap of these 76 differential proteins identified in EAU rats is shown...”
T106B_MOUSE / Q80X71 Transmembrane protein 106B from Mus musculus (Mouse) (see 8 papers)
XP_006505232 transmembrane protein 106B isoform X1 from Mus musculus
Aligns to 119:259 / 275 (51.3%), covers 100.0% of PF07092, 225.6 bits
- function: In neurons, involved in the transport of late endosomes/lysosomes (PubMed:25066864, PubMed:32160553). May be involved in dendrite morphogenesis and maintenance by regulating lysosomal trafficking (PubMed:25066864). May act as a molecular brake for retrograde transport of late endosomes/lysosomes, possibly via its interaction with MAP6 (By similarity). In motoneurons, may mediate the axonal transport of lysosomes and axonal sorting at the initial segment (PubMed:32160553). It remains unclear whether TMEM106B affects the transport of moving lysosomes in the anterograde or retrograde direction in neurites and whether it is particularly important in the sorting of lysosomes in axons or in dendrites (Probable). In neurons, may also play a role in the regulation of lysosomal size and responsiveness to stress (PubMed:25066864). Required for proper lysosomal acidification (PubMed:28728022).
subunit: Can form homomers (By similarity). Interacts (via N-terminus) with MAP6 (via C-terminus) (By similarity). Interacts (via C-terminus) with the vacuolar-type ATPase subunit ATP6AP1 (By similarity). Interacts (via N-terminus) with AP2M1 and CLTC (By similarity). Interacts with TMEM106C (By similarity).
disruption phenotype: Knockout mice are born at the expected Mendelian ratio and young animals appear phenotypically normal (PubMed:28728022, PubMed:29855382, PubMed:32160553, PubMed:32852886). At 10 weeks of age, knockout mice develop proximal axonal swellings caused by drastically enlarged LAMP1-positive vacuoles (lysosomes/endosomes), increased retrograde axonal transport of lysosomes, and accumulation of lipofuscin and autophagosomes. Giant vacuoles specifically accumulate at the distal end and within the axon initial segment, but not in peripheral nerves or at axon terminals, resulting in an impaired facial-nerve-dependent motor performance (PubMed:32160553, PubMed:32852886). Using a different experimental approach to create the knockout, a more subtle, exclusively lysosomal phenotype is observed. At 2 months of age, numerous lysosomal proteins, including cathepsin B/CTSB, cathepsin L/CTSL, dipeptidyl peptidase 2/DPP7, LAMP1 and vacuolar-type ATPase subunits, are down-regulated and lysosomal acidification is impaired (PubMed:28728022). It has been suggested that these phenotypic differences might be due to incomplete knockout in animals with milder phenotypes (PubMed:32160553). Mice deficient in both PGRN and TMEM106B are born at normal Mendelian frequency and do not show any obvious growth defects or body weight changes. At around 3.5 months of age, the animals develop severe ataxia, hindlimb weakness, reduced motor activity, altered clasping behavior and eventually premature death. Neuronal loss and severe microglia and astrocyte activation are observed in the spinal cord, retina, and brain (PubMed:32761777, PubMed:32852886, PubMed:32929860). Myelin degeneration occurs in the spinal cord (PubMed:32761777). Drastic autophagy and lysosomal abnormalities, as well as other pathological changes related to frontotemporal lobar degeneration (FTLD)/amyotrophic lateral sclerosis are observed (PubMed:32761777, PubMed:32852886, PubMed:32929860). Most studies consistently show that loss of TMEM106B exacerbates lysosome abnormalities found in GRN-single knockout animals, likely contributing to neuronal dysfunction and neuronal death (PubMed:32761777, PubMed:32852886, PubMed:32929860). However, one study reports that the expression levels of most lysosomal proteins are normalized in double knockout mice and comparable to those of wild-type animals and some behavioral phenotypes observed in GRN-single knockout mice, such as locomotor hyperactivity and disinhibition, are rescued in double knockout (PubMed:28728022). TMEM106B knockout does not rescue FTLD-like phenotypes in a mouse model mimicking the toxic gain-of- functions associated with overexpression of hexanucleotide repeat (GGGGCC) expansions in C9ORF72 (PubMed:29855382). - Lack of a protective effect of the Tmem106b "protective SNP" in the Grn knockout mouse model for frontotemporal lobar degeneration.
Cabron, Acta neuropathologica communications 2023 - GeneRIF: Lack of a protective effect of the Tmem106b "protective SNP" in the Grn knockout mouse model for frontotemporal lobar degeneration.
- TMEM106B regulates microglial proliferation and survival in response to demyelination.
Zhang, Science advances 2023 - GeneRIF: TMEM106B regulates microglial proliferation and survival in response to demyelination.
- TMEM106B deficiency impairs cerebellar myelination and synaptic integrity with Purkinje cell loss.
Feng, Acta neuropathologica communications 2022 - GeneRIF: TMEM106B deficiency impairs cerebellar myelination and synaptic integrity with Purkinje cell loss.
- Aged Tmem106b knockout mice display gait deficits in coincidence with Purkinje cell loss and only limited signs of non-motor dysfunction.
Stroobants, Brain pathology (Zurich, Switzerland) 2021 - GeneRIF: Aged Tmem106b knockout mice display gait deficits in coincidence with Purkinje cell loss and only limited signs of non-motor dysfunction.
- The FTLD Risk Factor TMEM106B Regulates the Transport of Lysosomes at the Axon Initial Segment of Motoneurons.
Lüningschrör, Cell reports 2020 (PubMed)- GeneRIF: The FTLD Risk Factor TMEM106B Regulates the Transport of Lysosomes at the Axon Initial Segment of Motoneurons.
- A role of the frontotemporal lobar degeneration risk factor TMEM106B in myelination.
Feng, Brain : a journal of neurology 2020 - GeneRIF: A role of the frontotemporal lobar degeneration risk factor TMEM106B in myelination.
- Loss of Tmem106b exacerbates FTLD pathologies and causes motor deficits in progranulin-deficient mice.
Zhou, EMBO reports 2020 - GeneRIF: Loss of Tmem106b exacerbates FTLD pathologies and causes motor deficits in progranulin-deficient mice.
- Loss of TMEM106B and PGRN leads to severe lysosomal abnormalities and neurodegeneration in mice.
Feng, EMBO reports 2020 - GeneRIF: Loss of TMEM106B and PGRN leads to severe lysosomal abnormalities and neurodegeneration in mice.
- More
- TMEM106B is a receptor mediating ACE2-independent SARS-CoV-2 cell entry
Baggen, Cell 2023 (no snippet) - Comparison of urine proteomes from tumor-bearing mice with those from tumor-resected mice.
Heng, PeerJ 2023 - “...Q91X17 Uromodulin P07911 2.80E03 2.092 O35657 Sialidase-1 Q99519 2.50E04 2.002 P0CG49 Polyubiquitin-B P0CG47 1.92E02 1.968 Q80X71 Transmembrane protein 106B Q9NUM4 6.97E05 1.949 Q60590 Alpha-1-acid glycoprotein 1 P02763 1.30E02 1.825 P81117 Nucleobindin-2 P80303 1.14E02 1.727 P18761 Carbonic anhydrase 6 P23280 4.58E02 1.541 Q07797 Galectin-3-binding protein Q08380 3.74E02...”
- Hepatic Proteomic Analysis of Selenoprotein T Knockout Mice by TMT: Implications for the Role of Selenoprotein T in Glucose and Lipid Metabolism.
Li, International journal of molecular sciences 2021 - “...intrinsically disordered NOTCH2-binding receptor 1-like homolog 0.0069 Q8VCH0 Acaa1b 1.4334 3-ketoacyl-CoA thiolase B, peroxisomal 0.0057 Q80X71 Tmem106b 1.4200 Transmembrane protein 106B 0.0133 P13516 Scd1 1.4148 Acyl-CoA desaturase 1 0.0033 Q9CR30 Josd2 1.3915 Josephin-2 0.0100 Q6P1E7 Primpol 1.3635 DNA-directed primase/polymerase protein 0.0301 Q9EQQ2 Yipf5 1.3481 Protein YIPF5...”
Q3ZC25 Transmembrane protein 106B from Bos taurus
Aligns to 119:259 / 275 (51.3%), covers 100.0% of PF07092, 224.3 bits
T106B_HUMAN / Q9NUM4 Transmembrane protein 106B from Homo sapiens (Human) (see 19 papers)
NP_060844 transmembrane protein 106B from Homo sapiens
Aligns to 118:258 / 274 (51.5%), covers 100.0% of PF07092, 224.1 bits
- function: In neurons, involved in the transport of late endosomes/lysosomes (PubMed:25066864). May be involved in dendrite morphogenesis and maintenance by regulating lysosomal trafficking (PubMed:25066864). May act as a molecular brake for retrograde transport of late endosomes/lysosomes, possibly via its interaction with MAP6 (By similarity). In motoneurons, may mediate the axonal transport of lysosomes and axonal sorting at the initial segment (By similarity). It remains unclear whether TMEM106B affects the transport of moving lysosomes in the anterograde or retrograde direction in neurites and whether it is important in the sorting of lysosomes in axons or in dendrites (By similarity). In neurons, may also play a role in the regulation of lysosomal size and responsiveness to stress (PubMed:25066864). Required for proper lysosomal acidification (By similarity).
function: (Microbial infection) Plays a role in human coronavirus SARS- CoV-2 infection, but not in common cold coronaviruses HCoV-229E and HCoV-OC43 infections. Involved in ACE2-independent SARS-CoV-2 cell entry. Required for post-endocytic stage of virus entry, facilitates spike-mediated membrane fusion. Virus attachment and endocytosis can also be mediated by other cell surface receptors.
subunit: Can form homomers (PubMed:23136129, PubMed:25066864). Interacts (via N-terminus) with MAP6 (via C-terminus) (PubMed:24357581). Interacts (via C-terminus) with the vacuolar-type ATPase subunit ATP6AP1 (PubMed:28728022). Interacts (via N-terminus) with AP2M1 and CLTC (PubMed:25066864). Interacts with TMEM106C (PubMed:25066864).
subunit: (Microbial infection) Interacts with SARS coronavirus-2/SARS- CoV-2 spike protein (via RBD domain). - Localized proteomic differences in the choroid plexus of Alzheimer's disease and epilepsy patients
Leitner, Frontiers in neurology 2023 - “...-value Fold change Increased MACROH2A1 Core histone macro-H2A.1 O75367 8.64E-08 1.8 TMEM106B Transmembrane protein 106B Q9NUM4 3.22E-06 18.9 ERLIN2 Erlin-2 O94905 4.23E-06 1.7 HIBADH 3-hydroxyisobutyrate dehydrogenase, mitochondrial P31937 4.35E-06 1.8 FBLN1 Fibulin-1 P23142 4.43E-06 2.8 VAPA Vesicle-associated membrane protein-associated protein A Q9P0L0 6.84E-06 1.4 TGM2 Protein-glutamine...”
- “...FDR of >5% are detailed in Supplementary Table 6 . TMEM106B validation and localization TMEM106B (Q9NUM4) was among the top 20 most significantly altered proteins when comparing AD vs. epilepsy ( Table 3 ) with the highest fold change at an 18.9-fold increase ( p =...”
- Scaling of an antibody validation procedure enables quantification of antibody performance in major research applications
Ayoubi, 2023 - TMEM106B is a receptor mediating ACE2-independent SARS-CoV-2 cell entry
Baggen, Cell 2023 (no snippet) - Transcriptome Profiling of Oncorhynchus mykiss Infected with Low or Highly Pathogenic Viral Hemorrhagic Septicemia Virus (VHSV).
Biasini, Microorganisms 2023 - “...exocyst complex component 3-like protein 4 Q17RC7 110497811 2.11 4.32 4.61 tmem106b transmembrane protein 106B-like Q9NUM4 110486388 1.65 1.56 2.98 Fluctuating- regulated spsb4a SPRY domain-containing SOCS box protein 4-like 070911-3 B0S5W3 110508890 1.34 1.71 2.70 mycbp C-Myc-binding protein-like 110496688 1.29 1.86 2.41 rnf217 probable E3 ubiquitin-protein...”
- TMEM106B Fibrils from FTLD Patients and Healthy Controls.
Greenwood, ACS chemical neuroscience 2023 - “...Figure 2. (A) Primary sequence and (B) structural organization of TMEM106B and lysosomal processing (Uniprot Q9NUM4). Residues in blue depict confirmed N-linked glycosylation sites....”
- Comparison of urine proteomes from tumor-bearing mice with those from tumor-resected mice.
Heng, PeerJ 2023 - “...2.092 O35657 Sialidase-1 Q99519 2.50E04 2.002 P0CG49 Polyubiquitin-B P0CG47 1.92E02 1.968 Q80X71 Transmembrane protein 106B Q9NUM4 6.97E05 1.949 Q60590 Alpha-1-acid glycoprotein 1 P02763 1.30E02 1.825 P81117 Nucleobindin-2 P80303 1.14E02 1.727 P18761 Carbonic anhydrase 6 P23280 4.58E02 1.541 Q07797 Galectin-3-binding protein Q08380 3.74E02 0.669 P06869 Urokinase-type plasminogen...”
- Amyloid fibrils in FTLD-TDP are composed of TMEM106B and not TDP-43
Jiang, Nature 2022 - “...Protein Group Accessions Position in TMEM106B # PSMs IonScore E-value m/z (Da) m/z (ppm) SAYVSYDVQK Q9NUM4 130140 3 39 0.0044 580.28595 +1.34 LNNISIIGPLDMK a M12(Oxidation) Q9NUM4 181193 722.39960 +6.35 FCTLISIK C2(Carbamidomethyl) Q9NUM4 213220 3 59 2.1e-005 491.27747 +3.89 YQYVDCGR C6(Carbamidomethyl) Q9NUM4 248255 3 34 0.0025 530.73291...”
- Systematic detection of functional proteoform groups from bottom-up proteomic datasets.
Bludau, Nature communications 2021 - “...indicated as horizontal bars. C Peptide profiles of the transmembrane protein 106B (TMEM106B, UniProt ID: Q9NUM4) in interphase. Peptides of the two assigned proteoform groups are colored in orange and blue. D Protein sequence plot for TMEM106B. Sequence coverage and position of the detected peptides of...”
- “...show the profile and sequence location for peptides of Transmembrane protein 106B (TMEM106B, UniProt ID: Q9NUM4), which has no annotated sequence variants or specific post-processing steps annotated in UniProt. Nevertheless, COPF identified two clearly distinguishable, assembly-specific proteoforms (Supplementary Fig. 4B ). In recent literature, we found...”
- More
- TMEM106B core deposition associates with TDP-43 pathology and is increased in risk SNP carriers for frontotemporal dementia.
Marks, Science translational medicine 2024 - GeneRIF: TMEM106B core deposition associates with TDP-43 pathology and is increased in risk SNP carriers for frontotemporal dementia.
- Accumulation of TMEM106B C-terminal fragments in neurodegenerative disease and aging.
Perneel, Acta neuropathologica 2023 (PubMed)- GeneRIF: Accumulation of TMEM106B C-terminal fragments in neurodegenerative disease and aging.
- C-terminal TMEM106B fragments in human brain correlate with disease-associated TMEM106B haplotypes.
T, Brain : a journal of neurology 2023 - GeneRIF: C-terminal TMEM106B fragments in human brain correlate with disease-associated TMEM106B haplotypes.
- Superresolution live-cell imaging reveals that the localization of TMEM106B to filopodia in oligodendrocytes is compromised by the hypomyelination-related D252N mutation.
Xing, Science China. Life sciences 2023 (PubMed)- GeneRIF: Superresolution live-cell imaging reveals that the localization of TMEM106B to filopodia in oligodendrocytes is compromised by the hypomyelination-related D252N mutation.
- TMEM106B is a receptor mediating ACE2-independent SARS-CoV-2 cell entry.
Baggen, Cell 2023 - GeneRIF: TMEM106B is a receptor mediating ACE2-independent SARS-CoV-2 cell entry.
- TMEM106B Fibrils from FTLD Patients and Healthy Controls.
Greenwood, ACS chemical neuroscience 2023 - GeneRIF: TMEM106B Fibrils from FTLD Patients and Healthy Controls.
- TMEM106B aggregation in neurodegenerative diseases: linking genetics to function.
Jiao, Molecular neurodegeneration 2023 - GeneRIF: TMEM106B aggregation in neurodegenerative diseases: linking genetics to function.
- The major TMEM106B dementia risk allele affects TMEM106B protein levels, fibril formation, and myelin lipid homeostasis in the ageing human hippocampus.
Lee, Molecular neurodegeneration 2023 - GeneRIF: The major TMEM106B dementia risk allele affects TMEM106B protein levels, fibril formation, and myelin lipid homeostasis in the ageing human hippocampus.
- More
Q8N353 Transmembrane protein 106B (Fragment) from Homo sapiens
Aligns to 158:298 / 314 (44.9%), covers 100.0% of PF07092, 223.2 bits
Q1LWC2 Transmembrane protein 106B from Danio rerio
Aligns to 114:254 / 267 (52.8%), covers 100.0% of PF07092, 217.4 bits
T106A_HUMAN / Q96A25 Transmembrane protein 106A from Homo sapiens (Human) (see 2 papers)
NP_001278515 transmembrane protein 106A isoform a from Homo sapiens
Aligns to 116:252 / 262 (52.3%), covers 100.0% of PF07092, 214.6 bits
T106A_MOUSE / Q8VC04 Transmembrane protein 106A from Mus musculus (Mouse) (see paper)
NP_659079 transmembrane protein 106A from Mus musculus
Aligns to 115:251 / 261 (52.5%), covers 100.0% of PF07092, 204.8 bits
Q3T144 Transmembrane protein 106C from Bos taurus
Aligns to 107:247 / 249 (56.6%), covers 100.0% of PF07092, 181.3 bits
T106C_HUMAN / Q9BVX2 Transmembrane protein 106C; Endoplasmic reticulum membrane protein overexpressed in cancer from Homo sapiens (Human) (see paper)
NP_001137314 transmembrane protein 106C isoform a from Homo sapiens
Aligns to 108:248 / 250 (56.4%), covers 100.0% of PF07092, 174.2 bits
Or search for genetic data about PF07092 in the Fitness Browser
by Morgan Price,
Arkin group
Lawrence Berkeley National Laboratory