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JMJD1A and c-Myc (Montrer MYC Protéines) levels are independent prognostic factors for cervical cancer patients
Data suggest a critical role for KDM3A in the PI3K (Montrer PIK3CA Protéines)/AP-1 (Montrer FOSB Protéines) oncogenic axis and propose a novel strategy for inhibition of KDM3A against liver tumor development under PI3K (Montrer PIK3CA Protéines) pathway activation.
The authors find that KDM3A promotes anoikis through transcriptional activation of BNIP3 (Montrer BNIP3 Protéines) and BNIP3L (Montrer BNIP3L Protéines), which encode pro-apoptotic proteins.
The KDM3A to PRM1 (Montrer PRM1 Protéines) 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 (Montrer MCAM Protéines) expression both through a direct mechanism, involving modulation of H3K9 methylation at the MCAM (Montrer MCAM Protéines) promoter, and an indirect mechanism, via the Ets1 (Montrer ETS1 Protéines) transcription factor.
JMJD1A promotes urinary bladder cancer progression by enhancing glycolysis through coactivation of HIF1alpha (Montrer HIF1A Protéines).
depletion of KDM3A was capable of reactivating mutated p53 (Montrer TP53 Protéines) to induce the expression of pro-apoptotic genes in breast cancer with mutant p53 (Montrer TP53 Protéines). 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 (Montrer MYC Protéines) 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 (Montrer JUN Protéines) 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 (Montrer ADRB1 Protéines)) and downstream targets including Ucp1 (Montrer UCP1 Protéines) 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 (Montrer ACTB Protéines) and gamma-tubulin (Montrer TUBG1 Protéines).
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 (Montrer SRY Protéines) 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 (Montrer LYZ Protéines)-9 on histone 3 (H3K9me2), the preferred substrate for KDM3A.
the Jmjd1a-controlled epigenetic histone modifications are crucial for Crem (Montrer CREM Protéines)-regulated gene expression and spermatogenesis
TSGA may modulate the function of ER71 (Montrer ETV2 Protéines) 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 (Montrer KDM4A Protéines), and KDM4C (Montrer KDM4C Protéines) were expressed before and after embryonic genome activation, whereas KDM5B (Montrer KDM5B Protéines) was mainly expressed during the blastocyst period.
The histone H3 (Montrer HIST3H3 Protéines) lysine 9 demethylase (Montrer MBD2 Protéines) KDM3A facilitates the Xenopus Neurog2 (Montrer NEUROG2 Protéines) 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