The of cells to H2O2. Therefore, Sepw1 plays beneficial

The mRNA expression of SEPW1 which
was down-regulated in Methylnonanoic acid compound (Figure 3) might indicate
its function with regard to liver fatty acid metabolism. The expression pattern
of the SEPW1 gene was consistent with the previous study of fatty acids
transcriptome profiling (Yu et al. 2013). These results suggested that
the SEPW1 has lower expressions Methylnonanoic acid. Since gene of SEPW1 is a
highly expressed and have major influence in muscle more than other tissue (Yao
et al. 2014), it may be one of the reasons why we could not identify any
significant relation with the Methylnonanoic acid pattern of SEPW1 and liver
tissue. Noh et al. (2010) has been reported that SelW mRNA stabilization
led to increase the expression level of SelW mRNA because of raise in
selenium-supplemented. Se supplementations have effect on modification of
fattyc acids by increasing the PUFAs content, particulary CLA isomers in liver
of lamb and its meat. Kubiak et al. (2016), stated that alter in Se
supply conduct singnificantly alter mRNA level of the genes and leads to
changes in the mRNA selenoproteins expression. Kubiak et al. (2016)
stated that changes in Se supply not only lead to changes in the mRNA
expression of selenoproteins but also significantly alter mRNA level of the
genes, SEPW1 playing important and major role in the fatty acids metabolism and
regulation of the triglycerides.

SelW expression it has been found to
work as regulated during C2C12 cell differentiation (Noh et al. 2010).
The mRNA level of SelW through the differentiation process of myoblasts and the
optimal Se concentrations for expression of SelW mRNA in chicken myoblasts is
10?7 M is influenced by Se( Ruan et al. 2012). Overexpression of SEPW
could decrease the H2O2- influence oxidative damage.furthermore, the increased
expression of certain antioxidative selenoproteins could regulate
oxidation–reduction homeostasis in cells, improve the ability of cells to save
against oxidative stress and reduce the oxidative damage and the concentration
of H2O2 (Yao et al. 2014).

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Overexpression of SelW experiment
indicated that it might play important role in component of the cellular
defense system against oxidative stress (Sun et al. 2001). Increased of
Malondialdehyde (MDA) levels found to be induced with SEPW1 deficiency, also it
is reported that Sepw1 deficiency reduced the ability of myoblasts to buffer
the exogenous H2O2 and increased the sensitivity of cells to H2O2. Therefore,
Sepw1 plays beneficial role in antioxidative functions in myoblasts also
indicating that Sepw1 and Gpx1 may play important roles in the response to
oxidative stress in chicken myoblasts. Therefore, chicken Sepw1 also preserves
antioxidative function (Yao et al. 2014). Selenoprotein deficiency
conducted to thereby suppressed T cell proliferation in response to T cell
receptor stimulation and oxidant hyperproduction of T cells. therfore, such a
redox function could present positive physiological benefit (Whanger 2009 ).
moreover, Selenoprotein deficiency also reduced the Sepw1 mRNA level in the
muscle (Li et al. 2011), our population were relied on pasture fed
without and additive feed or concentration, maybe there were some deficiency of
Se , for this reason, it should give Se supplementations in feed to avoid Se
deficiency. Transcripts of Selenoprotein found to be significantly and highly
down-regulated in liver, because of Se deficiency, in corresponding tissues Se
plays an essential role in conserving insulin function during the selenoprotein
regulation encoding gene (Xu et al. 2017).

SEPW1 (selenoprotein W-1)contains
SeCys (SeCys13), encoded by the UGA codon. SEPW1 belongs to the selenoprotein W
subfamily, of the selenoprotein WTH family, and functions as an antioxidant
enzyme. Specifically, SEPW1 binds to glutathione which targets reactive oxygen
species such as hydroxyl radical, hydrogen peroxide and superoxide anion
radical (Matthews et al. 2014). Amantana et al. (2002), reported
that metal-response element (MRE) is expressed in the SEPW promoter which is
activated by exposure to zinc and copper. A transcription factor, specificity
protein 1 (Sp1), bound to consent Sp1sequence in the SEPW promoter, also to the
MRE sequence it founded by An in vitro binding assay (Amantana et al. 2004).
In addition, another group observed the induction of the mouse SelW promoter by
cadmium in a liver-specific metal-responsive transcription factor 1 (MTF-1)
knock-out mouse model. MTF-1 is a zinc finger protein involved in the response
to various stress stimuli, such as heavy metals and oxidative stress, which
acts by binding to MRE consensus sequences in the promoters of its target
genes. MTF-1 may act as an activator or repressor of selenoprotein expression
via binding to MREs located in the promoters or coding regions of its target
genes (Noh et al. 2010).

In Raman et al. (2013), Sepw1
directly interacts with the beta and gamma isoforms of 14-3-3 proteins. Further,
siRNA knockdown of Sepw1 expression halts cell cycle progression and inhibits
epithelial cell proliferation via a p53- and p21-dependent mechanism (Hawkes
and Alkan 2011; Hawkes et al. 2012). Cell cycle arrest at the G1 stage
caused by Sepw1 knockdown is mediated by MKK4 and downstream MAPK signaling
(Hawkes and Alkan 2012). SEPW1 was implicated in cell cycle recovery from G2
seize influence by DNA damage (Park et al. 2012) it’s showed that Sepw1
is extensively expressed in synapses and neurons, and suggest translational
sepw1 regulation by the RNA-binding protein Staufen .

 To the best of our knowledge, no study has
investigated the asscociation and expression of SEPW1 gene with regard to the
production traits in livestock including sheep. SelW is able to bind reduced
glutathione (GSH) (Jeong et al. 2002). SelW is involved in redox
regulation during its interactions with 14-3-3 proteins, it is opined that SelW
is a member of the thioredoxin family (Hu et al. 2014). Sepw1 was
initially identified by its absence in muscle of myopathic lambs suffering
White Muscle disease, and later purified and cloned ( Whanger 2000).)
Production traits might have been influenced by the small study population. Therefore,
the experimental population size should be increased for future studies to avoid
such biases and obtain more precise data