Family Search for PF07092 (TMEM106)

PF07092 hits 10 sequences in PaperBLAST's database above the trusted cutoff. Showing hits to curated sequences only. Or see all hits 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).

T106B_MOUSE / Q80X71 Transmembrane protein 106B from Mus musculus (Mouse) (see 8 papers)
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).

T106B_HUMAN / Q9NUM4 Transmembrane protein 106B from Homo sapiens (Human) (see 19 papers)
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).

T106A_HUMAN / Q96A25 Transmembrane protein 106A from Homo sapiens (Human) (see 2 papers)
Aligns to 116:252 / 262 (52.3%), covers 100.0% of PF07092, 214.6 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:29131025, PubMed:30456879).

T106A_MOUSE / Q8VC04 Transmembrane protein 106A from Mus musculus (Mouse) (see paper)
Aligns to 115:251 / 261 (52.5%), covers 100.0% of PF07092, 204.8 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).

T106C_HUMAN / Q9BVX2 Transmembrane protein 106C; Endoplasmic reticulum membrane protein overexpressed in cancer from Homo sapiens (Human) (see paper)
Aligns to 108:248 / 250 (56.4%), covers 100.0% of PF07092, 174.2 bits

• subunit: Interacts with TMEM106B.

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