2016
DOI: 10.5603/fhc.a2016.0020
|View full text |Cite
|
Sign up to set email alerts
|

Knockdown of Sucla2 decreases the viability of mouse spermatocytes by inducing apoptosis through injury of the mitochondrial function of cells

Abstract: Introduction. Sucla2, a b subunit of succinyl coenzyme A synthase, is located in the mitochondrial matrix. Sucla2 catalyzes the reversible synthesis of succinate and adenosine triphosphate (ATP) in the tricarboxylic acid cycle. Sucla2 expression was found to be correlated with the capacitation of boar spermatozoa. We have previously reported that Sucla2 was decreased in the testes of rats with spermatogenesis failure after exposure to endocrine disruptor BDE47. Yet, the expression model of Sucla2 in spermatoge… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

0
1
0

Year Published

2018
2018
2022
2022

Publication Types

Select...
2

Relationship

0
2

Authors

Journals

citations
Cited by 2 publications
(1 citation statement)
references
References 35 publications
(53 reference statements)
0
1
0
Order By: Relevance
“…GOT2 also catalyzes the synthesis of α-ketoglutarate, which is the initial step for ATP production in the TCA cycle [ 78 , 79 ]. The synthesis of α-ketoglutarate from succinate is catalyzed by SUCLA2 [ 80 , 81 ]. However, stimulation of DLD can reduce α-ketoglutarate but increase succinate production [ 82 ], revealing that DLD up-regulation induced by high salinity stress in branchial cells may increase downstream metabolites of TCA cycle and promote mitochondrial ATP production.…”
Section: Discussionmentioning
confidence: 99%
“…GOT2 also catalyzes the synthesis of α-ketoglutarate, which is the initial step for ATP production in the TCA cycle [ 78 , 79 ]. The synthesis of α-ketoglutarate from succinate is catalyzed by SUCLA2 [ 80 , 81 ]. However, stimulation of DLD can reduce α-ketoglutarate but increase succinate production [ 82 ], revealing that DLD up-regulation induced by high salinity stress in branchial cells may increase downstream metabolites of TCA cycle and promote mitochondrial ATP production.…”
Section: Discussionmentioning
confidence: 99%