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The protein encoded by ATL1 is a GTPase and a Golgi body transmembrane protein. Additionally we are shipping ATL1 Proteins (7) and many more products for this protein.
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This study suggests that atlastin may regulate BMP receptor (show BMPR1A Antibodies) trafficking. and genetic or pharmacological inhibition of BMP signaling was sufficient to rescue the loss of mobility and spinal motor axon defects of atl1 morphants.
Variants in the ATL1 gene are a less frequent cause of hereditary spastic paraplegia among Czech patients than has been previously reported among other populations.
This study demonstrated that ATL1 gene mutation associated with hereditary spastic paraplegias in group of Polish patients
The results suggest that tethering and lipid mixing are catalyzed concurrently by atlastin GTPase (show RACGAP1 Antibodies) hydrolysis but that the energy requirement for lipid mixing exceeds that for tethering, and the full energy released through crossover formation is necessary for fusion.
that Atlastin 1 mutations may cause autosomal recessively inherited paraplegia with an underlying loss-of-function mechanism. Hence, patients with recessive forms of HSP should also be tested for the Atlastin 1 gene.
This study showed that the mutations of were detected in SPG11 (show SPG11 Antibodies), ATL1, NIPA1 (show NIPA1 Antibodies), and ABCD1 (show ABCD1 Antibodies) in patient with hereditary spastic paraplegia.
We identified two novel mutations and two previously reported mutations in SPAST (show SPAST Antibodies) and ATL1, respectively. The family with the ATL1 c.1204T>G mutation exhibited male-lethality, female infancy-onset, and pseudo- X-linked dominant transmission
Novel splicing pathogenic variants were identified in ATL1 genes of Korean patients with hereditary spastic paraplegia.
a deficit in the membrane fusion activity of atlastin1 may be a key contributor, but is not required, for hereditary spastic paraplegia causation.
These results suggest that the three ATLs have different capacities to mediate endoplasmic reticulum fusion, with ATL1 being the strongest and ATL3 (show ATL3 Antibodies) being the weakest.
purified and reconstituted human ATL1 exhibited no in vitro fusion activity. When the cytosolic segment of human ATL1 was connected to the transmembrane (TM) region and C-terminal tail (CT) of Drosophila ATL
Endoplasmic reticulum morphology is markedly disrupted in ATL1, ATL2 (show ATL2 Antibodies), and ATL3 (show ATL3 Antibodies) knockout cells.
VCP (valosin-containing protein (show vcp Antibodies)), together with its cofactor P47 (show MFGE8 Antibodies) and the endoplasmic reticulum (ER) morphology regulator ATL1 (Atlastin-1), regulates tubular ER formation
This publication discusses functional and mutational aspects of atlastin GTPase 1 in humans.
The protein encoded by this gene is a GTPase and a Golgi body transmembrane protein. The encoded protein can form a homotetramer and has been shown to interact with spastin and with mitogen-activated protein kinase kinase kinase kinase 4. This protein may be involved in axonal maintenance as evidenced by the fact that defects in this gene are a cause of spastic paraplegia type 3. Three transcript variants encoding two different isoforms have been found for this gene.
atlastin GTPase 1
, spastic paraplegia 3A (autosomal dominant)
, GTP-binding protein 3
, brain-specific GTP-binding protein
, guanine nucleotide-binding protein 3
, guanylate-binding protein 3
, spastic paraplegia 3 protein A
, spastic paraplegia 3A homolog