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JMJD1A and c-Myc (show MYC Proteins) levels are independent prognostic factors for cervical cancer patients
Data suggest a critical role for KDM3A in the PI3K (show PIK3CA Proteins)/AP-1 (show FOSB Proteins) oncogenic axis and propose a novel strategy for inhibition of KDM3A against liver tumor development under PI3K (show PIK3CA Proteins) pathway activation.
The authors find that KDM3A promotes anoikis through transcriptional activation of BNIP3 (show BNIP3 Proteins) and BNIP3L (show BNIP3L Proteins), which encode pro-apoptotic proteins.
The KDM3A to PRM1 (show PRM1 Proteins) mRNA expression ratio can be used as a reliable marker of successful testicular sperm extraction in men with obstructive and non-obstructive azoospermia with 95% sensitivity.
Authors show that KDM3A regulates MCAM (show MCAM Proteins) expression both through a direct mechanism, involving modulation of H3K9 methylation at the MCAM (show MCAM Proteins) promoter, and an indirect mechanism, via the Ets1 (show ETS1 Proteins) transcription factor.
JMJD1A promotes urinary bladder cancer progression by enhancing glycolysis through coactivation of HIF1alpha (show HIF1A Proteins).
depletion of KDM3A was capable of reactivating mutated p53 (show TP53 Proteins) to induce the expression of pro-apoptotic genes in breast cancer with mutant p53 (show TP53 Proteins). KDM3A knockdown also potently inhibited tumorigenic potentials of breast cancer stem-like cells and rendered them sensitive to apoptosis induced by chemotherapeutic drugs.
our findings reveal a novel mechanism by which KDM3A promotes ovarian CSCs, proliferation and chemoresistance and thus, highlights the significance of KDM3A as a novel therapeutic target for resistant ovarian cancer.
a critical role for JMJD1A in regulating proliferation and survival of prostate cancer cells by controlling c-Myc (show MYC Proteins) expression at transcriptional and post-translational levels
deficient expression of JMJD1A/JMJD1A might be reflecting and/or contributing to round spermatid maturation arrest
Data suggest a critical role for KDM3A in the PI3K/AP-1 (show JUN Proteins) oncogenic axis and propose a novel strategy for inhibition of KDM3A against liver tumor development under PI3K pathway activation.
JMJD1A is phosphorylated at S265 by protein kinase A (PKA), and this is pivotal to activate the beta1-adrenergic receptor gene (Adrb1 (show ADRB1 Proteins)) and downstream targets including Ucp1 (show UCP1 Proteins) in brown adipocytes.
Kdm3a localizes to cytoplasmic structures of maturing spermatids affected in Kdm3a mutant mice, which in turn display altered fractionation of beta-actin (show ACTB Proteins) and gamma-tubulin (show TUBG1 Proteins).
Results show that Jmjd1a was not essential for stem cell self-renewal but played a crucial role as a tumor suppressor.
Despite these differences in rats, genetic knockout of Kdm3a in mice resulted in no dramatic effect on immune system development and activation or EAE susceptibility and severity
Jmjd1a directly and positively controls Sry (show SRY Proteins) expression by regulating H3K9me2 marks. These studies reveal a pivotal role of histone demethylation in mammalian sex determination.
Exposing cells to either chemical or cellular sources of (*)NO resulted in a significant increase in dimethyl Lys (show LYZ Proteins)-9 on histone 3 (H3K9me2), the preferred substrate for KDM3A.
the Jmjd1a-controlled epigenetic histone modifications are crucial for Crem (show CREM Proteins)-regulated gene expression and spermatogenesis
TSGA may modulate the function of ER71 (show ETV2 Proteins) and thereby affect spermatogenesis as well as embryonic development
Jmjd1a might be a critical signaling molecule underlying the maintenance of pluripotency in mouse embryonic stem cells
Histone demethylases KDM3A, KDM4A (show KDM4A Proteins), and KDM4C (show KDM4C Proteins) were expressed before and after embryonic genome activation, whereas KDM5B (show KDM5B Proteins) was mainly expressed during the blastocyst period.
The histone H3 (show HIST3H3 Proteins) lysine 9 demethylase (show MBD2 Proteins) KDM3A facilitates the Xenopus Neurog2 (show NEUROG2 Proteins) chromatin accessibility during neuronal transcription. Loss-of-function analyses reveal that KDM3A is not required for the transition of naive ectoderm to neural progenitor cells but is essential for primary neuron formation.
This gene encodes a zinc finger protein that contains a jumonji domain and may play a role in hormone-dependent transcriptional activation. Alternative splicing results in multiple transcript variants.
jmjC domain-containing histone demethylation protein 2A
, jumonji C domain-containing histone demethylase 2A
, jumonji domain containing 1
, jumonji domain containing 1A
, jumonji domain-containing protein 1A
, lysine-specific demethylase 3A
, testis-specific protein A
, lysine (K)-specific demethylase 3A
, testis specific gene A
, probable zinc finger protein
, testis-specific gene A protein
, zinc finger protein TSGA
, lysine-specific demethylase 3A-like
, jumonji domain-containing protein 1A-B
, lysine-specific demethylase 3A-B
, LOW QUALITY PROTEIN: lysine-specific demethylase 3A