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1 or channels mediate Zn(2+) influx throughout folliculogenesis.
2 be potentially related to egg production and folliculogenesis.
3 ctivate MISR2 signaling and suppress ovarian folliculogenesis.
4 ovaries and, when ablated in mice, perturbed folliculogenesis.
5 n the ovary during oocyte cyst breakdown and folliculogenesis.
6 released by eEPCs into CM, were crucial for folliculogenesis.
7 is severely defective at multiple stages of folliculogenesis.
8 maintenance and differentiation during early folliculogenesis.
9 of GATA4 and FOG2 in ovarian development and folliculogenesis.
10 id they contribute to oocytes during de novo folliculogenesis.
11 re oocyte-specific and detectable throughout folliculogenesis.
12 n of Pou5f1 and Gdf9 in oocytes during early folliculogenesis.
13 risome protein candidates that may influence folliculogenesis.
14 e polyovular follicles, suggesting a role in folliculogenesis.
15 of gonad development-germ cell migration and folliculogenesis.
16 fringe-deficient ovary demonstrated aberrant folliculogenesis.
17 ling pathway and lunatic fringe in mammalian folliculogenesis.
18 a highly regulated expression pattern during folliculogenesis.
19 chromosome disorganization without affecting folliculogenesis.
20 em most likely plays a pivotal role in early folliculogenesis.
21 early as one-layer follicles and throughout folliculogenesis.
22 hogenetic proteins (BMPs) in early stages of folliculogenesis.
23 ding how oocyte growth factors contribute to folliculogenesis.
24 atrix and the oolemma, that perturbed normal folliculogenesis.
25 not PP1gamma, in oocytes from all stages of folliculogenesis.
26 ins (matrisome), and its role in controlling folliculogenesis.
27 tor-9 (GDF-9), which is required for ovarian folliculogenesis.
28 rmal ovarian function and egg production via folliculogenesis.
29 in mammals undergo cyclic development during folliculogenesis.
30 ther they are expressed uniformly throughout folliculogenesis.
31 s FSH expression and results in a failure of folliculogenesis.
32 RT1(-/-) ovaries did not undergo meiosis and folliculogenesis.
34 showed that reconstituted ovaries exhibited folliculogenesis after transplantation of PGCs-aggregate
35 promotes an ovarian environment defective in folliculogenesis and conducive to teratoma formation.
36 ound that Calr fcKO female mice had impaired folliculogenesis and decreased ovulatory rates due to de
37 ies have revealed key roles of the oocyte in folliculogenesis and established that bidirectional comm
40 Given the importance of FSH in regulating folliculogenesis and fertility, the development of FSH m
44 epithelial basement membrane is crucial for folliculogenesis and is controlled by endothelial cell i
47 ity, the direct effects of FSH glycoforms on folliculogenesis and oocyte quality were determined usin
49 atic follicle cells of the ovary to regulate folliculogenesis and ovulation in mammals; however, thei
50 ovary, they play important roles in ovarian folliculogenesis and ovulation, whereas in the male repr
52 ed exclusively in oocytes throughout most of folliculogenesis and play central roles in controlling o
53 llicles within the ovary, but their roles in folliculogenesis and pregnancy, as well as the necessity
54 s an increase in EGFR expression during late folliculogenesis and provide evidence that the FSH-depen
55 ary homeobox gene) deficiency disrupts early folliculogenesis and the expression of oocyte-specific g
56 pecific genes, including those that initiate folliculogenesis and those that encode the zona pellucid
58 f key hallmarks of oocyte development during folliculogenesis, and highlight UBE2I as a previously un
59 creasing cell-to-cell communication early in folliculogenesis, and that the shift in in vivo abundanc
61 nesis) and their enclosure by somatic cells (folliculogenesis) are processes not limited to the perin
62 d an essential role for insulin signaling in folliculogenesis as conditional ablation of Igf1r in pri
63 pe of BMP-15-null mice, which exhibit normal folliculogenesis but have defects in the ovulation proce
64 Static images provide a thumbnail view of folliculogenesis but imperfectly capture the dynamic cel
65 abnormal zona matrix does not affect initial folliculogenesis, but there is a significant decrease in
66 of oocyte meiotic progression and primordial folliculogenesis by decreasing intra-oocyte cAMP levels.
68 ions in oocyte-GC communication during early folliculogenesis can induce GCT by activating an autocri
69 viable but infertile because of a defect in folliculogenesis correlating with restricted expression
70 thelial progenitor cells (eEPCs) rescued the folliculogenesis defects of both Smad1/5(dKO) and Vegfa(
73 yte can help us better understand oogenesis, folliculogenesis, fertilization, and embryonic developme
74 n is required in the mammalian oocyte during folliculogenesis for both oocyte development and communi
75 multitude of signaling pathways required for folliculogenesis have been identified, downstream transc
76 of both Egfr and EGFR increases during late folliculogenesis in Fshb(+/-) females, these increases f
80 ntified similarities and differences between folliculogenesis in the native microenvironment and the
81 ion of a subset of genes required for proper folliculogenesis in the ovary and establishes TAFII105 a
85 demonstrates normal thecal layer, defects in folliculogenesis including many degenerating antral foll
89 its identification as a regulator of ovarian folliculogenesis, its use in fertility clinics as a meas
92 ation of two genes that are known to disrupt folliculogenesis: newborn ovary homeobox gene (Nobox) an
94 Unique for the ovary, hormonally regulated folliculogenesis, ovulation, luteal formation/regression
95 ient females are infertile due to a block in folliculogenesis prior to antral follicle formation.
96 evelopment and lactation, failure of ovarian folliculogenesis resulting in decreased fertility, loss
98 roteins (ZP1, ZP2, ZP3) that are involved in folliculogenesis, species-specific fertilization, and pa
99 otropins during the endocrine stimulation of folliculogenesis (superovulation) may contribute to the
100 own to be co-expressed in oocytes throughout folliculogenesis, supporting the idea that BMP-15 is a p
101 s between granulosa cells and oocytes during folliculogenesis that are critical to maximize developme
104 naling and endothelial cell invasion promote folliculogenesis via assembly of the basement membrane.
105 th mutant PI3K-positive oocytes during early folliculogenesis were essential for the GC transformatio
106 n completely abrogates this wounding-induced folliculogenesis, whereas overexpression of Wnt ligand i