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The results displayed that INSL3 changed RXFP2 expression in mouse gubernaculum testis cells in vitro
COUP-TFII cooperates with the nuclear receptor steroidogenic factor 1 (SF1) to further enhance Insl3 promoter activity in Leydig cells.
Microarray expression profiling of whole adrenal mRNA from ovariectomized vs. intact mice demonstrated selective upregulation of gonadal-like genes including Spinlw1 and Insl3 in GDX-induced adrenocortical tumors of the mouse.
Our data suggest that beta-catenin and NOTCH1 pathways are potential targets of INSL3 signaling during gubernacular development.
Data suggest that Insl3/Rxfp2 (insulin-like peptide 3/relaxin receptor 2) signaling is important for testicular descent; however, germ-cell deletion of Rxfp2 did not affect spermatogenesis, germ cell survival, or male fertility.
beta-catenin and Notch pathways are potential targets of INSL3 signaling during gubernacular development.
INSL3 is a powerful and multifunctional promoter of tumor growth and angiogenesis in human thyroid cancer cell xenografts. INSL3 actions involve RXFP2 activation and the secretion of S100A4 and (pro-)cathepsin-L
Poorly formed gubernacula and increased testicular mobility in Insl3 mutant mice result in spermatic cord anomalies, delayed/absent testicular descent and subsequent testicular torsion in a gene dose dependent manner
overexpression of the insl3 in female mice causes descent of the ovaries
Mutations in INSL3 might contribute to the etiology of cryptorchidism.I
Insl3 expression causes inguinal hernia in females; gubernaculum formation is the most sensitive biological response as regards Insl3
Disruption of the Greatgene causes failure of the transabdominal phase of descent, identical to that seen in the Insl3-deficient mutants, consistent with the recent data suggesting that Great gene encodes the Insl3 transmembrane receptor.
neither Insl3 nor Lgr8 contribute to the RLN signaling pathway; Insl3/Lgr8 and Rln1/Lgr7 actions do not overlap in vivo
Insl3/Lgr8 and Rln1/Lgr7 pathways are distinct and separate in vivo
NR4A1 as an important regulator of mouse INSL3 promoter activity
Important new insights into the regulation of Insl3 transcription in Leydig cells and the mode of action of phthalates.
These results suggest that the downregulation of INSL3 mRNA by diethylhexyl phthalate might cause abnormalities of gubernacular development, which might be one of the mechanisms for development of cryptorchidism.
INSL3 evidently traverses the blood-testis barrier to enter the seminiferous compartment, rete testis, and epididymis in sufficient concentration to be able to address the specific INSL3 receptors (RXFP2) on post-meiotic germ cells and in the epididymis.
Estradiol represses Insl3 expression in MA-10 Leydig cells.
Variants of the INSL3 gene are prevalent in patients with testicular torsion instead of healthy subjects.
The strong positive correlation between INSL3, and high ovarian androgens levels in all polycystic ovary syndrome women, which appeared clearly in undescended polycystic ovaries could support the proposed syndrome hypothesis between those abnormal findings.
KLF6-mediated activation of the human INSL3 promoter required an intact KLF element as well as Leydig/Sertoli-enriched factors. KLF6 transcriptionally cooperates with NUR77 and SF1. our results identify KLF6 as a regulator of human INSL3 transcription.
The INSL3 G178A polymorphism was not significantly associated with spermatozoa or no spermatozoa in the testes of males with a history of bilateral cryptorchidism. I The evidence suggests that mutations of INSL3 may not directly contribute to the damage of spermatogenesis in patients with bilateral cryptorchidism history.
hINSL3 seems to recruit Aund spermatogonia into differentiation, potentially mediating an Fsh effect on spermatogenesis.
Healthy eumenorrheic late adolescent females with sporadic anovulation display higher INSL3 blood concentration.
rs6523 polymorphism and AGAG haplotype of INSL3 showed significant association with increased risk of polycystic ovary syndrome.
INSL3 in girls is a unique and specific marker of theca cells surrounding antral follicles.
Three common INSL3 gene polymorphisms (27G>A, 126G>A, 178G>A) unrelated to any particular phenotype of testicular maldescent (TMD) were detected both in patients and controls, indicating that INSL3 gene mutations are not a common cause of TMD.
DLK1, INSL3 and COUP-TFII expression changes during normal development and is linked to different stages of Leydig Cell differentiation.
low INSL3 concentration is related to the pathogenesis behind an unfavourable change in body composition and bone metabolism among Klinefelter syndrome patients
The aim of this study was to assess plasma INSL3 in patients with osteoporosis and Klinefelter's Syndrome compared to healthy males.
INSL3 is as sensitive a marker as T for the evaluation of altered Leydig cell function in congenital hypogonadotropic hypogonadism/Kallmann syndrome patients.
INSL3 and AMH levels are significantly correlated with each other in women with PCOS, and they are significantly increased, particularly in the presence of amenorrhea and oligomenorrhea.
Findings suggest a novel and gender-specific role for INSL3 and cognate receptor RXFP2 signaling in ocular surface homeostasis.
Most Prader-Willi syndrome males have normal INSL3 levels.
In the meta-analysis, INSL3 rs10421916 and rs11088680 had both a 0.8-fold decreased odds ratio for gastric cancer.
Cystin A11-B10 serves as an insulator between the two ports, whereas the amide functionality disturbs the signal transmission complex likely due to changes in polarity.
Data suggest that insulin-like factor 3 is related to functional ovarian hyperandrogenism in women with polycystic ovary syndrome.
study demonstrates that the INSL3/RXFP2 system is involved in bone metabolism by acting on the MAPK cascade and stimulating transcription of important genes of osteoblast maturation/differentiation and osteoclastogenesis
This study thus provides evidence for substantial transfer of INSL3 between fetuses, and probably also across the placenta, emphasizing the vulnerability of the fetus to extrinsic hormonal influences within the uterus.
RXFP2 was expressed in boar meiotic and post-meiotic germ cells, where INSL3 neutralization led to increased germ cell apoptosis and reduced sperm output, suggesting that INSL3 acts as a survival/anti-apoptotic factor in maintaining sperm production.
The study suggests the existence of RLF/INSL3-RXFP2 signaling in germ cells of boars.
Circulating INSL3 was shown to increase progressively during development
These results indicate that boar RLF/INSL3 is secreted from testicular Leydig cells as a B-C-A monomeric structure with full biological activity.
insl3 gene SNPs can be excluded as a common genetic basis for hernia inguinalis in pigs
These results suggest that reduced secretions of IGF-I, INSL3, and inhibin surrounding puberty may be associated with semen aberration in beef bulls.
These results suggested an acute regulation of INSL3 by luteinizing hormone (LH) because INSL3 concentrations increased immediately after endogenous and exogenous LH stimulation.
INSL3 plays a luteotropic role as a local regulator in the bovine corpus luteum.
BMP6 has a role in downregulating INSL3 and CYP17A1 and other proteins that modulate ovarian androgen production
The likely role of INSL3 as an important intrafollicular modulator of thecal interna cell function/steroidogenesis.
INSL3 provides the first example of a gender-specific fetal hormone with the potential to influence both placental and maternal physiology
relaxin-like factor mRNA was highly expressed in the corpus luteum on days 7 and 14 of pregnancy
This gene encodes a member of the insulin-like hormone superfamily. The encoded protein is mainly produced in gonadal tissues. Studies of the mouse counterpart suggest that this gene may be involved in the development of urogenital tract and female fertility. This protein may also act as a hormone to regulate growth and differentiation of gubernaculum, and thus mediating intra-abdominal testicular descent. Mutations in this gene may lead to cryptorchidism. Alternate splicing results in multiple transcript variants.
, Ley I-L
, leydig insulin-like peptide
, relaxin like factor
, relaxin-like factor
, Leydig insulin-like peptide relaxin-like factor
, leydig insulin -like hormone
, relaxin-like factor b
, insulin-like factor 3
, Leydig insulin-like hormone
, insulin-like peptide-3
, insulin-like 3 (Leydig cell)
, insulin-like peptide 3
, insulin-like 3-like
, Insulin-like 3
, Relaxin-like factor
, Leydig insulin-like peptide