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BOLL belongs to the DAZ gene family required for germ cell development. Additionally we are shipping BOLL Proteins (5) and many more products for this protein.
Showing 10 out of 105 products:
Human Polyclonal BOLL Primary Antibody for ELISA, IHC - ABIN268678
Lin, Chung, Cheng: Posttranscriptional regulation of CDC25A by BOLL is a conserved fertility mechanism essential for human spermatogenesis. in The Journal of clinical endocrinology and metabolism 2009
Show all 2 Pubmed References
Human Polyclonal BOLL Primary Antibody for ELISA - ABIN547140
Xu, Moore, Pera: A gene family required for human germ cell development evolved from an ancient meiotic gene conserved in metazoans. in Proceedings of the National Academy of Sciences of the United States of America 2001
Four sterility-related genes, including BOLL, DDX4, HORMAD1, and MAEL, were found to have increased methylation at CpGs of the promoter regions and decreased mRNA expressions in nonobstructive azoospermia and hypospermatogenesis (HS) testis and are believed to be associated with HS.
hypermethylation of DAZL and BOULE promoters in human sperm is associated with human infertility
Our study demonstrated an oncogenic role of BOLL in CRC despite tumor-specific promoter hypermethylation.
demonstrate that Boll is also transiently expressed during oogenesis in the fetal mouse ovary, but is simultaneously co-expressed within the same germ cells as Dazl
Assessing the expression of both CDY1 and BOULE by qualitative RT-PCR is a sensitive and feasible test for predicting the presence of sperm cells in testicular tissue biopsies.
expression of spermatogenic phenotypes of partial AZFc deletions is independent of the variations in DAZL and BOULE in the Han population
BOULE may encode a key conserved switch that regulates progression of germ cells through meiosis in men.
Role in spermatogenesis. Decreased DAZ proteins in spermatogenic failure may be due to germ cell loss. Transcription of BOULE, DAZL, and DAZ not altered in degrees of spermatogenic failure. No increase of DAZL or BOULE found in DAZ deletion.
Major group of infertile men with meiotic arrest lack BOULE protein and its putative target, CDC25A expression. Spermatogenic failure may arise from factor(s) upstream of BOULE possibly involved in regulating transcription and/or translation of BOULE.
BOULE coding sequence mutations are not an important factor in the aetiology of azoospermia.
mutations in BOULE can be eliminated as a major cause of impaired spermatogenesis.
Among the three BOULE isoforms, B2 might have the major role for meiotic completion.
CDC25A is subject to translational control by BOLL, which is an evolutionarily conserved mechanism.
human DAZL (deleted in azoospermia-like) functions in primordial germ-cell formation, whereas closely related genes DAZ and BOULE (also called BOLL) promote later stages of meiosis and development of haploid gametes
methylation status of the core promoter might be involved in testicular bBoule transcription
The b-boule gene is predicted to encode a polypeptide of 295 amino acids with an RNP-type RNA recognition domain. Tertiary structure analysis shows that b-boule binds specifically to polypyrimidine RNAs.
asked whether BOULE, the founding member of DAZ family proteins, is a component of the SGs. We show that BOULE is recruited to the SGs upon heat stress, and that these SGs are developmental stage-specific
These results showed that IGF1 regulated the expression of BOULE and CDC25A mRNAs via ERK1/2 signaling and in T-independent pathway during spermatogenesis in the adult mouse testes.
Expression of key regulators of spermiogenesis was unaffected in Boule(-/-) mice, suggesting that Boule regulates germ-cell differentiation through a novel pathway.
This gene belongs to the DAZ gene family required for germ cell development. It encodes an RNA-binding protein which is more similar to Drosophila Boule than to human proteins encoded by genes DAZ (deleted in azoospermia) or DAZL (deleted in azoospermia-like). Loss of this gene function results in the absence of sperm in semen (azoospermia). Histological studies demonstrated that the primary defect is at the meiotic G2/M transition. Two alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.