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S9075

Sigma-Aldrich

Anti-Synemin (N-terminal) antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

Sinónimos:

Anti-DMN, Anti-Desmuslin, Anti-SYN, Anti-SYNM

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~170 kDa

species reactivity

rat, human

technique(s)

immunohistochemistry: 1:150-1:300 using human skeletal muscle
western blot: 1:500-1:1000 using rat skeletal muscle extract (S1 fraction)

UniProt accession no.

O15061

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... SYNM(23336)
mouse ... Synm(233335)

Physical form

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Daniela Rodler et al.
Cells, tissues, organs, 197(4), 298-311 (2013-02-09)
In the present study, we examined the distribution of 6 groups of intermediate filaments (IFs; cytokeratins, CKs, vimentin, synemin, desmin, glial fibrillary acidic protein and lamins) in oocytes and follicular walls of the Japanese quail (Coturnix japonica) during their development
Taiji Tsunemi et al.
Human molecular genetics, 23(11), 2791-2801 (2013-12-18)
Mutations in ATP13A2 (PARK9) cause Kufor-Rakeb syndrome (KRS) characterized by juvenile-onset parkinsonism, pyramidal signs and dementia. PARK9 belongs to type 5 P-type ATPase with its putative function as a cation transporter. Loss of PARK9 leads to lysosomal dysfunction and subsequent
Giulia Romano et al.
Neurobiology of disease, 71, 95-109 (2014-08-05)
Alterations in TDP-43 are commonly found in patients suffering from amyotrophic lateral sclerosis (ALS) and the genetic suppression of the conserved homologue in Drosophila (TBPH) provokes alterations in the functional organization of motoneuron synaptic terminals, resulting in locomotive defects and
Hayat Banoujaafar et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 34(10), 1681-1687 (2014-07-24)
We investigated the contribution of blood flow elevation in the cerebrovasculature to physical training-induced brain-derived neurotrophic factor (BDNF) levels elevation in the brain. Brain-derived neurotrophic factor protein levels were measured in the motor cortex 24 h after the last session of
Ramon Guirado et al.
The international journal of neuropsychopharmacology, 17(10), 1635-1646 (2014-05-03)
Novel hypotheses suggest that antidepressants, such as the selective serotonin reuptake inhibitor fluoxetine, induce neuronal structural plasticity, resembling that of the juvenile brain, although the underlying mechanisms of this reopening of the critical periods still remain unclear. However, recent studies

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