Family Search for PF07092 (DUF1356)

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 28:259 / 275 (84.4%), covers 97.4% of PF07092, 399.9 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 28:259 / 275 (84.4%), covers 97.8% of PF07092, 399.9 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).
• 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.
• Loss of TMEM106B potentiates lysosomal and FTLD-like pathology in progranulin-deficient mice.
  Werner, EMBO reports 2020
  • GeneRIF: Loss of TMEM106B potentiates lysosomal and FTLD-like pathology in progranulin-deficient mice.
• Progranulin and TMEM106B: when two become wan.
  Clayton, EMBO reports 2020
  • GeneRIF: Progranulin and TMEM106B: when two become wan.
• More
• 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...”

T106B_HUMAN / Q9NUM4 Transmembrane protein 106B from Homo sapiens (Human) (see 18 papers)
NP_060844 transmembrane protein 106B from Homo sapiens
Aligns to 27:258 / 274 (84.7%), covers 97.8% of PF07092, 399.0 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) May act as a proviral host factor for SARS-CoV-2, but not for common cold coronaviruses HCoV-229E and HCoV- OC43.
  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).
• Death Receptor 5 (TNFRSF10B) Is Upregulated and TRAIL Resistance Is Reversed in Hypoxia and Normoxia in Colorectal Cancer Cell Lines after Treatment with Skyrin, the Active Metabolite of Hypericum spp.
  Babinčák, Cancers 2021
  • “...2.06 0 1.37 0 Q16850 Lanosterol 14-alpha demethylase (GN = CYP51A1) 1.84 0 1.33 0 Q9NUM4 Transmembrane protein 106B (GN = TMEM106B) 1.34 0.01 1.66 0.01 H3BU86 STX16-NPEPL1 readthrough (NMD candidate) (GN = STX16-NPEPL1) 1.8 0.02 1.18 0.05 Q8ND82 Zinc finger protein 280C (GN = ZNF280C)...”
• 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...”
• Proteomic distinction of renal oncocytomas and chromophobe renal cell carcinomas.
  Drendel, Clinical proteomics 2018
  • “...reductase) (Putative sterol reductase SR-1) (Sterol C14-reductase) (Transmembrane 7 superfamily member 2) 1.92 0.05 0.01 Q9NUM4 Transmembrane protein 106B 0.71 0.38 0.00 Q12792 Twinfilin-1 (Protein A6) (Protein tyrosine kinase 9) 0.40 1.13 0.00 O15498 Synaptobrevin homolog YKT6 (EC 2.3.1.-) Fig.2 a Statistical analysis using linear models...”
• TMEM106B in humans and Vac7 and Tag1 in yeast are predicted to be lipid transfer proteins.
  Levine, Proteins 2022 (PubMed)
  • GeneRIF: TMEM106B in humans and Vac7 and Tag1 in yeast are predicted to be lipid transfer proteins.
• Homotypic fibrillization of TMEM106B across diverse neurodegenerative diseases.
  Chang, Cell 2022
  • GeneRIF: Homotypic fibrillization of TMEM106B across diverse neurodegenerative diseases.
• Amyloid fibrils in FTLD-TDP are composed of TMEM106B and not TDP-43.
  Jiang, Nature 2022 (PubMed)
  • GeneRIF: Amyloid fibrils in FTLD-TDP are composed of TMEM106B and not TDP-43.
• Age-dependent formation of TMEM106B amyloid filaments in human brains.
  Schweighauser, Nature 2022
  • GeneRIF: Age-dependent formation of TMEM106B amyloid filaments in human brains.
• TMEM106B Acts as a Modifier of Cognitive and Motor Functions in Amyotrophic Lateral Sclerosis.
  Manini, International journal of molecular sciences 2022
  • GeneRIF: TMEM106B Acts as a Modifier of Cognitive and Motor Functions in Amyotrophic Lateral Sclerosis.
• Identification of TMEM106B amyloid fibrils provides an updated view of TMEM106B biology in health and disease.
  Perneel, Acta neuropathologica 2022
  • GeneRIF: Identification of TMEM106B amyloid fibrils provides an updated view of TMEM106B biology in health and disease.
• A novel temporal-predominant neuro-astroglial tauopathy associated with TMEM106B gene polymorphism in FTLD/ALS-TDP.
  Llibre-Guerra, Brain pathology (Zurich, Switzerland) 2021
  • GeneRIF: A novel temporal-predominant neuro-astroglial tauopathy associated with TMEM106B gene polymorphism in FTLD/ALS-TDP.
• rs1990622 variant associates with Alzheimer's disease and regulates TMEM106B expression in human brain tissues.
  Hu, BMC medicine 2021
  • GeneRIF: rs1990622 variant associates with Alzheimer's disease and regulates TMEM106B expression in human brain tissues.
• More

Q8N353 TMEM106B protein (Fragment) from Homo sapiens
Aligns to 67:298 / 314 (73.9%), covers 97.8% of PF07092, 397.9 bits

• Pharmacoproteomic analysis reveals that metapristone (RU486 metabolite) intervenes E-cadherin and vimentin to realize cancer metastasis chemoprevention
  Yu, Scientific reports 2016
  • “...4 0.517* 97 277 18.2 P81605-2 Isoform 2 of Dermcidin 4 0.606* 98 263 19.1 Q8N353 TMEM106B protein 5 0.399* 99 1189 34.5 Q53G71 Calreticulin variant 11 0.601* 100 395 20.9 Q13217 DnaJ homolog subfamily C member 3 5 0.374* 101 126 17.4 B2RE34 cDNA, FLJ96901...”

Q3ZC25 Transmembrane protein 106B from Bos taurus
Aligns to 28:259 / 275 (84.4%), covers 97.4% of PF07092, 397.6 bits

• Quantitative proteomic analysis shows involvement of the p38 MAPK pathway in bovine parainfluenza virus type 3 replication.
  Li, Virology journal 2022
  • “...Q9TTM7 Antigen processing and presentation Extracellular matrix;cytoplasmic part Binding 0.033 0.582 27 Transmembrane protein 106B Q3ZC25 Developmental process; Cell morpho-genesis Membrane; Cytoplasm 0.002 0.582 28 Uncharacterized protein E1BM92 Single-multicellular organism process Plasma membrane region; Cytoplasm Cytoskeletal protein binding 0.041 0.588 29 Mitochondrial ribonuclease P protein 1...”

Q1LWC2 Transmembrane protein 106B from Danio rerio
Aligns to 24:254 / 267 (86.5%), covers 96.6% of PF07092, 387.3 bits

• Gonadal transcriptomics elucidate patterns of adaptive evolution within marine rockfishes (Sebastes)
  Heras, BMC genomics 2015
  • “...0.008 0.008 1.068 486 Q62348 2.08E-78 Q62348 9.20E-58 transmembrane protein 106b 0.019 0.011 1.817 360 Q1LWC2 1.23E-18 Q1LWC2 1.28E-25 transmembrane protein 50a 0.053 0.035 1.518 279 O95807 1.58E-65 O95807 3.27E-37 trna guanosine-2 -o-methyltransferase trm11 homolog 0.036 0.021 1.704 285 Q05B63 2.25E-57 Q7TNK6 7.43E-34 tumor necrosis factor...”

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 25:252 / 262 (87.0%), covers 99.1% of PF07092, 374.2 bits

• function: Activates macrophages and polarizes them into M1-like macrophages through the activation of the MAPK and NF-kappaB signaling pathway. Upon activation, up-regulates the expression of CD80, CD86, CD69 and MHC II on macrophages, and induces the release of pro- inflammatory cytokines such as TNF, IL1B, IL6, CCL2 and nitric oxide (By similarity). May play a role in inhibition of proliferation and migration (PubMed:30456879, PubMed:29131025).
• Transmembrane protein 106A is silenced by promoter region hypermethylation and suppresses gastric cancer growth by inducing apoptosis.
  Xu, Journal of cellular and molecular medicine 2014
  • GeneRIF: Low TMEM106A expression is associated with gastric cancer.

T106A_MOUSE / Q8VC04 Transmembrane protein 106A from Mus musculus (Mouse) (see paper)
NP_659079 transmembrane protein 106A from Mus musculus
Aligns to 24:251 / 261 (87.4%), covers 99.6% of PF07092, 370.2 bits

• function: Activates macrophages and polarizes them into M1-like macrophages through the activation of the MAPK and NF-kappaB signaling pathway (PubMed:26215746). Upon activation, up-regulates the expression of CD80, CD86, CD69 and MHC II on macrophages, and induces the release of pro-inflammatory cytokines such as TNF, IL1B, IL6, CCL2 and nitric oxide (PubMed:26215746). May play a role in inhibition of proliferation and migration (By similarity).
• Inactivation of TMEM106A promotes lipopolysaccharide-induced inflammation via the MAPK and NF-κB signaling pathways in macrophages.
  Zhang, Clinical and experimental immunology 2021
  • GeneRIF: Inactivation of TMEM106A promotes lipopolysaccharide-induced inflammation via the MAPK and NF-kappaB signaling pathways in macrophages.
• Transmembrane protein 106a activates mouse peritoneal macrophages via the MAPK and NF-κB signaling pathways.
  Dai, Scientific reports 2015
  • GeneRIF: data suggest that mouse Tmem106a might be a new trigger of macrophage activation and have some influence toward the M1 state through the activation of the MAPKs and NF-kappaB pathway

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 17:248 / 250 (92.8%), covers 99.1% of PF07092, 333.9 bits

• subunit: Interacts with TMEM106B.
• TMEM106C contributes to the malignant characteristics and poor prognosis of hepatocellular carcinoma.
  Duan, Aging 2021
  • GeneRIF: TMEM106C contributes to the malignant characteristics and poor prognosis of hepatocellular carcinoma.
• LINC00238 inhibits hepatic carcinoma progression by activating TMEM106C‑mediated apoptosis pathway.
  Jiang, Molecular medicine reports 2021
  • GeneRIF: LINC00238 inhibits hepatic carcinoma progression by activating TMEM106Cmediated apoptosis pathway.
• Transmembrane protein 106C promotes the development of hepatocellular carcinoma.
  Luo, Journal of cellular biochemistry 2020 (PubMed)
  • GeneRIF: Transmembrane protein 106C promotes the development of hepatocellular carcinoma.

Q3T144 Transmembrane protein 106C from Bos taurus
Aligns to 17:247 / 249 (92.8%), covers 98.7% of PF07092, 333.6 bits

• Integrated multi-omics analyses reveals molecules governing sperm metabolism potentially influence bull fertility
  Talluri, Scientific reports 2022
  • “...GULO l -gulonolactone oxidase 5.8 l -ascorbic acid biosynthetic process Top ten downregulated proteins 1. Q3T144 TMEM106C Transmembrane protein 106C 3.93 Integral component of Endoplasmic reticulum, facilitates sperm motility 2. O18883 TXNDC9 Thioredoxin domain-containing protein 9 3.35 Microtubule organization, protection against oxidative stress 3. Q08DX7 SPNS1...”

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