ArticleMolecular biology of the cell2002
Regulation of IkappaBbeta expression in testis.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 37 citations in OpenAlex.
- Genome-wide identification and annotation of SNPs and their mapping in candidate genes related to milk production and fertility traits in Badri cattle.Tropical animal health and production · 2023Article
- Association study between single-nucleotide variants rs12097821, rs2477686, and rs10842262 and idiopathic male infertility risk in Serbian population with meta-analysis.Journal of assisted reproduction and genetics · 2020Article
- Genome-wide discovery of SNPs in candidate genes related to production and fertility traits in Sahiwal cattle.Tropical animal health and production · 2020Article
- PEX10, SIRPA-SIRPG, and SOX5 gene polymorphisms are strongly associated with nonobstructive azoospermia susceptibility.Journal of assisted reproduction and genetics · 2019Article
- Expression profiles of Sox transcription factors within the postnatal rodent testes.Molecular and cellular biochemistry · 2018Article
- Transcriptional regulation of human sperm-associated antigen 16 gene by S-SOX5.BMC molecular biology · 2017Article
- Expressions of Sox9, Sox5, and Sox13 transcription factors in mice testis during postnatal development.Molecular and cellular biochemistry · 2015Article
- Haploinsufficiency of SOX5 at 12p12.1 is associated with developmental delays with prominent language delay, behavior problems, and mild dysmorphic features.Human mutation · 2012Article
- A genome-wide association study in Chinese men identifies three risk loci for non-obstructive azoospermia.Nature genetics · 2011Article
- Transcriptional regulation of an axonemal central apparatus gene, sperm-associated antigen 6, by a SRY-related high mobility group transcription factor, S-SOX5.The Journal of biological chemistry · 2010Article
- Anthrax lethal toxin enhances IkappaB kinase activation and differentially regulates pro-inflammatory genes in human endothelium.The Journal of biological chemistry · 2009Article
- In vivo binding of NF-kappaB to the IkappaBbeta promoter is insufficient for transcriptional activation.The Biochemical journal · 2006Article
- ERV3 and related sequences in humans: structure and RNA expression.Journal of virology · 2005Article
- RelA/p65 regulation of IkappaBbeta.Molecular and cellular biology · 2005Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
IkappaBalpha and IkappaBbeta are regulators of the nuclear factor-kappaB (NF-kappaB) transcription factor family. Both IkappaBs bind to the same NF-kappaB dimers and are widely expressed in different cells and tissues. To better understand how these two IkappaB isoforms differ biologically, we have characterized the expression of IkappaBbeta in testis, a tissue in which IkappaBalpha is only minimally expressed. We have found that IkappaBbeta expression is localized within the haploid spermatid stages of spermatogenesis and follows the expression of nuclear NF-kappaB. IkappaBbeta expression in haploid spermatids is likely regulated by Sox family proteins, members of which are also expressed within spermatids. We have shown that both SRY and Sox-5 can bind to multiple Sox binding sites found within the IkappaBbeta promoter and can enhance transcription of a reporter gene in transient transfection assays. We also demonstrate that IkappaBbeta mRNA is strongly expressed in developing male gonads. These results therefore suggest that IkappaBbeta may be a novel target for transcription factors of the HMG-box SRY/Sox family and imply a potential role for NF-kappaB/IkappaBbeta in spermatogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.