Nuclear factor-kappa-B-inhibitor alpha (NFKBIA) is a developmental marker of NF- B/p65 activation during in vitro oocyte maturation and early embryogenesis

Paciolla, Mariateresa; Boni, Raffaele; Fusco, Francesca; Pescatore, Alessandra; Poeta, Loredana; Ursini, Mv; Lioi, Maria Brigida; Miano, Maria Giuseppina

doi:10.1093/humrep/der040

Cited by 42 publications

(30 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It has been reported that the cAMP-PKA pathway is involved in ZGA and also the subsequent embryo development [46,47]. A recent report has also demonstrated the increase in DNA binding activity of NF-κB in bovine embryo, suggesting that NF-κB might be involved in ZGA [48]. In the present study, we have shown that HCO 3 − activates cAMP-PKA and NF-κB through CFTR and sAC, suggesting that HCO 3 − may be involved in the regulation of ZGA via the CFTR/ sAC/PKA/NF-κB pathway, apart from its involvement in the epigenetic regulation of p53 latency.…”

Section: Discussionmentioning

confidence: 95%

CFTR mediates bicarbonate-dependent activation of miR-125b in preimplantation embryo development

et al. 2012

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 95%

CFTR mediates bicarbonate-dependent activation of miR-125b in preimplantation embryo development

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Total RNA was used to make cDNA using Superscript III First Strand Synthesis System for RT-PCR (Invitrogen). Steady-state mRNA abundance was determined by real-time PCR by using Power SYBR Green PCR Master Mix (Applied Biosystems, Waltham, MA, USA) on the 7900HT Fast Real Time PCR System (Applied Biosystems, Foster City, CA, USA), as described elsewhere, 45 using the following primers: Icam1 (5′-TTCACACTGAATGCCAGCTC-3′; 3′-GTCTGCTGAGACCCCTCTTG-5′); Nfkbia (5′-CTGCAGGCCACCAACTACAA-3′ 3′-CAGCACCCAAAGTCACCAAGT-5′); Hprt (5′-GGCTTACCTCACTGCTTTCC-3′ 5′-CTGGTTCATCATCGCTAATCAC-3′).…”

Section: Methodsmentioning

confidence: 99%

NEMO regulates a cell death switch in TNF signaling by inhibiting recruitment of RIPK3 to the cell death-inducing complex II

et al. 2016

View full text Add to dashboard Cite

Incontinentia Pigmenti (IP) is a rare X-linked disease characterized by early male lethality and multiple abnormalities in heterozygous females. IP is caused by NF-κB essential modulator (NEMO) mutations. The current mechanistic model suggests that NEMO functions as a crucial component mediating the recruitment of the IκB-kinase (IKK) complex to tumor necrosis factor receptor 1 (TNF-R1), thus allowing activation of the pro-survival NF-κB response. However, recent studies have suggested that gene activation and cell death inhibition are two independent activities of NEMO. Here we describe that cells expressing the IP-associated NEMO-A323P mutant had completely abrogated TNF-induced NF-κB activation, but retained partial antiapoptotic activity and exhibited high sensitivity to death by necroptosis. We found that robust caspase activation in NEMO-deficient cells is concomitant with RIPK3 recruitment to the apoptosis-mediating complex. In contrast, cells expressing the ubiquitin-binding mutant NEMO-A323P did not recruit RIPK3 to complex II, an event that prevented caspase activation. Hence NEMO, independently from NF-κB activation, represents per se a key component in the structural and functional dynamics of the different TNF-R1-induced complexes. Alteration of this process may result in differing cellular outcomes and, consequently, also pathological effects in IP patients with different NEMO mutations.

show abstract

“…During murine spermatogenesis, NFκB is activated in a stage-specific manner (Lilienbaum et al, 2000). During oocyte maturation and early embryonic development, NFκB is activated (Nishikimi et al, 1999; Paciolla et al, 2011). In Drosophila melanogaster , the mRNA of the p65 homolog, named Dorsal, is maternally expressed and is concentrated in the egg cortex (Chen et al, 2000).…”

Section: Nfκb Signaling In Embryonic Neurogenesis (Neurodevelopment)mentioning

confidence: 99%

NFκB signaling regulates embryonic and adult neurogenesis

Zhang

2012

Front. Biol.

View full text Add to dashboard Cite

Both embryonic and adult neurogenesis involves the self-renewal/proliferation, survival, migration and lineage differentiation of neural stem/progenitor cells. Such dynamic process is tightly regulated by intrinsic and extrinsic factors and complex signaling pathways. Misregulated neurogenesis contributes much to a large range of neurodevelopmental defects and neurodegenerative diseases. The signaling of NFκB regulates many genes important in inflammation, immunity, cell survival and neural plasticity. During neurogenesis, NFκB signaling mediates the effect of numerous niche factors such as cytokines, chemokines, growth factors, extracellular matrix molecules, but also crosstalks with other signaling pathways such as Notch, Shh, Wnt/β-catenin. This review summarizes current progress on the NFκB signaling in all aspects of neurogenesis, focusing on the novel role of NFκB signaling in initiating early neural differentiation of neural stem cells and embryonic stem cells.

show abstract

Nuclear factor-kappa-B-inhibitor alpha (NFKBIA) is a developmental marker of NF- B/p65 activation during in vitro oocyte maturation and early embryogenesis

Cited by 42 publications

References 67 publications

CFTR mediates bicarbonate-dependent activation of miR-125b in preimplantation embryo development

CFTR mediates bicarbonate-dependent activation of miR-125b in preimplantation embryo development

NEMO regulates a cell death switch in TNF signaling by inhibiting recruitment of RIPK3 to the cell death-inducing complex II

NFκB signaling regulates embryonic and adult neurogenesis

Contact Info

Product

Resources

About