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SNAP29, a member of the SNAP25 gene family, encodes a protein involved in multiple membrane trafficking steps. Additionally we are shipping SNAP29 Proteins (5) and many more products for this protein.
Showing 10 out of 50 products:
Rat (Rattus) Polyclonal SNAP29 Primary Antibody for IHC, WB - ABIN350910
Pabst, Hazzard, Antonin, Suedhof, Jahn, Rizo, Fasshauer: Selective interaction of complexin with the neuronal SNARE complex. Determination of the binding regions. in The Journal of biological chemistry 2000
Show all 2 references for ABIN350910
Human Polyclonal SNAP29 Primary Antibody for IP, WB - ABIN1742239
Wilhelm, Mandad, Truckenbrodt, Kröhnert, Schäfer, Rammner, Koo, Claßen, Krauss, Haucke, Urlaub, Rizzoli: Composition of isolated synaptic boutons reveals the amounts of vesicle trafficking proteins. in Science (New York, N.Y.) 2014
Human Polyclonal SNAP29 Primary Antibody for ELISA, WB - ABIN564029
Sprecher, Ishida-Yamamoto, Mizrahi-Koren, Rapaport, Goldsher, Indelman, Topaz, Chefetz, Keren, Obrien, Bercovich, Shalev, Geiger, Bergman, Horowitz, Mandel et al.: A mutation in SNAP29, coding for a SNARE protein involved in intracellular trafficking, causes a novel neurocutaneous syndrome characterized by cerebral dysgenesis, neuropathy, ichthyosis, and ... in American journal of human genetics 2005
Human Monoclonal SNAP29 Primary Antibody for IF, ELISA - ABIN564030
Pattu, Qu, Schwarz, Strauss, Weins, Bhat, Halimani, Marshall, Rettig, Hoth: SNARE protein expression and localization in human cytotoxic T lymphocytes. in European journal of immunology 2012
SNAP29 gene contributes to the epidermal differentiation.
We suggest that Rab3A (show RAB3A Antibodies) may regulate SNAP-29-mediated membrane fusion during myelination.
phenotypic variability in Arab families with c.223delG mutation affected by cerebral dysgenesis, neuropathy, ichthyosis (show LBR Antibodies) and keratoderma syndrome
support a role of Snap29 at key steps of membrane trafficking, and predict that signaling defects may contribute to the pathogenesis of cerebral dysgenesis
In mammalian cells, mutating the O-GlcNAc (show OGT Antibodies) sites in SNAP-29, promotes the formation of a SNAP (show NAPA Antibodies)-29-containing SNARE (show NAPA Antibodies) complex, increases fusion between autophagosomes and endosomes/lysosomes, and promotes autophagic flux.
This work implicates SNAP29 as a major modifier of variable expressivity in 22q11.2 DS patients.
a causal relationship between defective function of SNAP29 and the pleiotropic manifestations of CEDNIK syndrome
SNAP29 mediated membrane fusion has an important role in endocytic recycling and consequently, in cell motility
SNAP-29 acts as a negative modulator for neurotransmitter release, probably by slowing recycling of the SNARE (show NAPA Antibodies)-based fusion machinery and synaptic vesicle turnover
a SNAP29 mutation codes for a SNARE (show NAPA Antibodies) protein involved in intracellular trafficking and causes a novel neurocutaneous syndrome characterized by cerebral dysgenesis, neuropathy, ichthyosis (show LBR Antibodies), and palmoplantar keratoderma
This gene, a member of the SNAP25 gene family, encodes a protein involved in multiple membrane trafficking steps. Two other members of this gene family, SNAP23 and SNAP25, encode proteins that bind a syntaxin protein and mediate synaptic vesicle membrane docking and fusion to the plasma membrane. The protein encoded by this gene binds tightly to multiple syntaxins and is localized to intracellular membrane structures rather than to the plasma membrane. While the protein is mostly membrane-bound, a significant fraction of it is found free in the cytoplasm. Use of multiple polyadenylation sites has been noted for this gene.
synaptosomal-associated protein, 29kDa
, synaptosomal-associated protein 29
, soluble 29 kDa NSF attachment protein
, vesicle-membrane fusion protein SNAP-29
, golgi SNARE of 32 kDa
, synaptosomal-associated protein 29kD
, synaptosomal-associated protein, 29kD