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Loss of EAAT4 (zeige SLC1A6 Antikörper) accounts for the initial hyper-excitability of Purkinje cells lacking b-III spectrin and that loss of GLAST (zeige SLC1A3 Antikörper) appears to work synergistically to worsen motor deficits. When levels of both EAAT4 (zeige SLC1A6 Antikörper) and GLAST (zeige SLC1A3 Antikörper) are compromised in b-III(-/-) mice, the proximal dendrites of Purkinje cells within the posterior cerebellum are the most vulnerable to degeneration.
TGF-beta (zeige TGFB1 Antikörper)/beta2-spectrin/CTCF (zeige CTCF Antikörper)-regulated tumor suppression in human stem cell disorder Beckwith-Wiedemann syndrome.
Study shows a direct interaction between beta-III spectrin and erythroid ankyrin (zeige ANK1 Antikörper) in the cerebellum and to demonstrate a critical role for beta-III spectrin in maintaining ankyrin R (zeige ANK1 Antikörper) throughout the Purkinje cell dendritic tree.
This study demonistrated that beta-III spectrin is critical for development of purkinje cell dendritic tree and spine morphogenesis.
Beta-III spectrin mutation L253P interferes with binding to Arp1 (zeige APOBEC2 Antikörper) and protein trafficking from the Golgi.
betaIII spectrin disruption impairs synaptogenesis by disturbing the intracellular pathways selectively regulating protein trafficking to the synapse
Cardiac beta2-spectrin and downstream molecules are regulated in multiple forms of cardiovascular disease via Ca(2+)- and calpain-dependent proteolysis.
This study indicates that high-affinity actin binding of L253P beta-III-spectrin is a likely driver of neurodegeneration.
beta2-Spectrin, a TGF-beta (zeige TGFB1 Antikörper) mediator and signaling molecule, is cleaved and activated by caspase-3 (zeige CASP3 Antikörper)/7, consequently enhancing apoptosis and transcriptional control to determine cell fate upon liver damage.
investigated using either targeted next generation sequencing or trio (zeige TRIO Antikörper)-based exome sequencing and were found to have mutations in three different genes, KCNC3 (zeige KCNC3 Antikörper), ITPR1 (zeige ITPR1 Antikörper) and SPTBN2
First Japanese spinocerebellar ataxia type 5 (SCA5) family with a novel heterozygous three-nucleotide in-frame deletion mutation in the SPTBN2 gene.
A homozygous SPTBN2 nonsense mutation underlying infantile ataxia and psychomotor delay in a human family.
Mutant beta-III spectrin causes mislocalization and dysfunction of mGluR1alpha at dendritic spines.
A novel missense mutation within a SPTBN2 spectrin repeat encoded by exon 12 was found in a family with spinocerebellar ataxia type 5.
the identification of SPARCA1 and normal heterozygous carriers of the stop codon in SPTBN2 provides insights into the mechanism of molecular dominance in SCA5 and demonstrates that the cell-specific repertoire of spectrin subunits
Spectrins are principle components of a cell's membrane-cytoskeleton and are composed of two alpha and two beta spectrin subunits. The protein encoded by this gene (SPTBN2), is called spectrin beta non-erythrocytic 2 or beta-III spectrin. It is related to, but distinct from, the beta-II spectrin gene which is also known as spectrin beta non-erythrocytic 1 (SPTBN1). SPTBN2 regulates the glutamate signaling pathway by stabilizing the glutamate transporter EAAT4 at the surface of the plasma membrane. Mutations in this gene cause a form of spinocerebellar ataxia, SCA5, that is characterized by neurodegeneration, progressive locomotor incoordination, dysarthria, and uncoordinated eye movements.
, spectrin beta 3
, spectrin beta chain, brain 2
, beta-III spectrin
, glutamate transporter EAAT4-associated protein 41
, spectrin beta chain, non-erythrocytic 2
, spectrin, non-erythroid beta chain 2
, spinocerebellar ataxia 5 protein
, beta SpIII sigma 1
, spectrin-like protein GTRAP41