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anti-Mouse (Murine) INSL3 Antibodies:
anti-Rat (Rattus) INSL3 Antibodies:
anti-Human INSL3 Antibodies:
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Human Polyclonal INSL3 Primary Antibody for IHC, IHC (p) - ABIN4326002
Nygaard, Almstrup, Lindbæk, Christensen, Svingen: Cell context-specific expression of primary cilia in the human testis and ciliary coordination of Hedgehog signalling in mouse Leydig cells. in Scientific reports 2015
Show all 3 Pubmed References
The results displayed that INSL3 changed RXFP2 (show RXFP2 Antibodies) expression in mouse gubernaculum testis cells in vitro
COUP-TFII (show NR2F2 Antibodies) cooperates with the nuclear receptor steroidogenic factor 1 (SF1 (show NR5A1 Antibodies)) 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 (show UBL4A Antibodies)-induced adrenocortical tumors of the mouse.
Our data suggest that beta-catenin (show CTNNB1 Antibodies) and NOTCH1 (show NOTCH1 Antibodies) pathways are potential targets of INSL3 signaling during gubernacular development.
Data suggest that Insl3/Rxfp2 (show RXFP2 Antibodies) (insulin-like peptide 3/relaxin receptor 2 (show RXFP2 Antibodies)) signaling is important for testicular descent; however, germ-cell deletion of Rxfp2 (show RXFP2 Antibodies) did not affect spermatogenesis, germ cell survival, or male fertility.
beta-catenin (show CTNNB1 Antibodies) and Notch (show NOTCH1 Antibodies) 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
KLF6 (show KLF6 Antibodies)-mediated activation of the human INSL3 promoter required an intact KLF element as well as Leydig/Sertoli-enriched factors. KLF6 (show KLF6 Antibodies) transcriptionally cooperates with NUR77 (show NR4A1 Antibodies) and SF1 (show NR5A1 Antibodies). our results identify KLF6 (show KLF6 Antibodies) 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 (show BRD2 Antibodies) 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 (show TTN Antibodies)) were detected both in patients and controls, indicating that INSL3 gene mutations are not a common cause of TMD (show TTN Antibodies).
DLK1 (show DLK1 Antibodies), INSL3 and COUP-TFII (show NR2F2 Antibodies) 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.
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 (show RXFP2 Antibodies) 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 (show RXFP2 Antibodies) 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 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 (show BMP6 Antibodies) has a role in downregulating INSL3 and CYP17A1 (show CYP17A1 Antibodies) 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