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Table 3 A list of differentially expressed proteins in the prefrontal cortex with fundamental roles in the regulation of cell death

From: Proteome profiling of different rat brain regions reveals the modulatory effect of prolonged maternal separation on proteins involved in cell death-related processes

Protein ID Gene name Protein name J S/C M S/C F S/C C M/F S M/F Protein function
Pdk2 [Pyruvate dehydrogenase (acetyl-transferring)] kinase isozyme 2, mitochondrial ↓ (0.35) p53 activation decreases Pdk2 transcription [92]
P97570 Pla2g6 85/88 kDa calcium independent phospholipase A2 S tBID and Bax augments Pla2g6 (iPLA2) activity via ROS production leading to changes in the MOM [93]
Overexpression of iPLA2 increased the rate of apoptosis, iPLA2 is cleaved by caspase-3 [94]
         β-cell apoptosis is attributable to the modulation of 5′SS selection in Bcl-X pre-mRNA by bioactive lipids modulated by iPLA2 [95]
Bax Apoptosis regulator BAX N C F Pro-apoptotic member of Bcl-2 family, its activation permeabilizes the MOM during apoptosis [96]
Deletion of Bax is sufficient to inhibit apoptosis [97]
Bax is cleaved by active calpains [80]
Bcl2l1 Bcl-2-like protein 1 C Bcl2l1 (Bcl-X) gene generates two protein products by alternative pre-mRNA splicing: Bcl-XL is anti-apoptotic, while Bcl-XS is pro-apoptotic; deletion of Bcl-X in mice results in neuronal death in the brain during late embryonic development; Bcl-XL overexpression attenuates brain injury in neonatal rodents [77]
Q91XJ1 Becn1 Beclin-1 N C F N Beclin-1-induced autophagy is inversely correlated with apoptosis [13]
Q6IN33 Rcan1 Calcipressin-1 C N C F N Calcineurin regulation; Rcan1 absence enhances calcineurin activity and Fas ligand expression [98]
Cast Calpastatin S N S N F Cast is a specific endogenous inhibitor of calpains and is cleaved by caspases [99]
P55213 Casp3 Caspase-3 S C F M Ceavage and activation of caspase-3 initiates apoptosis; essential for neuronal cell death [100]
Caspase-3 expression is regulated with age [21]
A regulatory calpain/caspase-3 cross-talk [101]
Q1HL14 Cers1 Ceramide synthase 1 S N N M Inhibition of de novo ceramide synthesis inhibited caspase 3/7 activation and apoptosis [102]
Overexpression of CerS1 and increased level of C18 ceramide resulted in activation of ER stress and inhibition of cell viability, independent of Bax [103]
Diablo LOC100360940 Diablo homolog S C F Diablo is located in the intermembrane space of mitochondria and is released into the cytosol during apoptosis and thereby enabling the activation of caspases [104]
Q8R2E7 Fadd FAS-associated death domain protein S S N Pro-apoptotic adapter protein involved in extrinsic pathway of apoptosis [100]
Overexpression of FADD promotes apoptosis [104]
Grid2 Glutamate ionotropic receptor, delta-2 C C C ↓ (0.47) Gain-to-function mutation of Grid2 induces neuronal death [105]; this mutation is associated with increased expression of Bax, Bcl-XS, caspase-3 and -8 [106]
TNF-α has a role in regulation of Grid2 gene expression, which can be a suppressor in TNF-induced neurodegeneration [107]
Grik2 Glutamate ionotropic receptor, kainate 2 N S F Grik2 (GluR6) promotes Bax translocation and increase in caspase-3 activation [108]
Q8VH49 Higd1a HIG1 domain family 1A, mitochondrial S S N N M Higd1a is a survival factor and is associated with caspase-3 activation [109, 110]
F1MAL5 Irs2 Insulin receptor substrate 2 N C N M N CaMK4/CREB/IRS2 cascade can inhibit apoptosis [111]
IRS2 knockout increased cell death and activation of caspase-3 and -8 as well as the levels of Fadd, Bcl-2, Bcl-XL and p53 [112]
P31423 Grm4 Metabotropic glutamate receptor 4 C C N Decreased expression of GRM4 gene is associated with apoptosis of cerebellar granule neurons [86]
Activation of Grm4 can activate pro-caspase 8/9/3 and disrupt the balance of Bcl-2/Bax expression [113]
P06907 Mpz Myelin protein P0 N C N M N Mpz knockdown induced apoptosis [114]
P2rx7 P2X purinoceptor 7 S ↓ (0.39) ↑ (3.28) P2rx7s mediate caspase-8 and caspase-3 dependent apoptosis [115]
Its activation is associated with Ca2+ responses and TNF-α production [116,117,118]
Mpv17 Protein Mpv17 S C C N The increase of Mpv17 expression can be accompanied by the enhanced expression of p53, Bax, cyt c and active caspase-3 and decreased expression of Bcl-2 in the pathological proces [119]
B1WC67 Slc25a24 RCG29001 S F A survival factor, knock-down of Slc25a24 led to reduction of Ca2+ buffering capacity and sensitized cellts to cell death induced by mitochondrial permeability transition [120]
Q63259 Ptprn Receptor–type tyrosine protein phosphatase-like N C M Ptprn knock-down can prevent apoptosis [121]
Q63639 Aldh1a2 Retinal dehydrogenase 2 N ↓ (0.36) Aldh1a2 mediates conversion of retinol into active retinoic acid altering the expression of Bcl-2, Bax, Bid, caspase-8 and -3 [122]
D4ADQ1 Rrm2b Ribonucleotide reductase M2 B (TP53 inducible) N S C F M Loss of Rrm2b can increase apoptosis [123]
Rrm2b expression is induced by stress [124]
Rrm2b cleavage is mediated by caspase-8 and -3 [125]
Rbm10 RNA-binding protein 10 C S C F M Rbm10 knock-down can decrease caspase activation [126]
Rbm10 regulates alternative splicing of Fas and Bcl-X genes [127]
Rbm10 expression is associated with increased apoptosis [128]
Stat5b;Stat5a Signal transducer and activator of transcription S S N N M Stat5 regulate expression of Bcl-2 and Bcl-XL and the level of caspase-3 [129,130,131]
Tnfaip8 TNF-α induced protein 8 N S F Tnfaip8 can suppress TNF-mediated apoptosis by inhibiting TNF-induced caspase-8 activity [69]
Tp53bp2 Tumor protein p53-binding protein 2 S S F Tp53bp2 binds to p53 and Bcl-2; it can alter p53 protein conformation and enhance the binding activity of p53 to the promotes of Bax [132]
  1. C protein detected only in samples of the cerebral cortex from control rats, S protein detected only in samples of the cerebral cortex from maternally separated rats, M protein detected only in samples of the cerebral cortex from adult male rats, F protein detected only in samples of the cerebral cortex from adult female rats, N protein not detected in the samples, –, unchanged protein expression between the samples; ↓, protein down-regulated in samples of the cerebral cortex from maternally separated rats; ↑, protein up-regulated in samples of the cerebral cortex from maternally separated rats