ライフサイエンスコーパス: FSH-beta

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1 n/monomeric subunit, because a CG beta alpha/FSH beta complex was also detected implying that triple

2 the CG beta subunit or the CG beta alpha and FSH beta monomer.

3 the stimulatory action of CREB to attenuate FSH beta transcription at high GnRH pulse frequencies, t

4 rast to the alpha and LH beta subunit genes, FSH beta subunit transcription is preferentially stimula

5 CG single chain interacts with the monomeric FSH beta subunit and exhibits FSH activity.

6 , GnRH receptor, and LH beta-subunit but not FSH beta-subunit).

7 rably photoaffinity-labels FSH alpha but not FSH beta.

8 is in contrast to photoaffinity labeling of FSH beta by the peptide mimic of the N-terminal region o

9 Ovariectomy led to increased amounts of FSH-beta but not LH-beta messenger RNA, which suggested

10 nd GnRH pulse frequency-dependent effects on FSH beta transcription.

11 Previously, we showed that the CG beta or FSH beta subunit genes can be genetically fused to the a

12 d for association with either the LH beta or FSH beta subunits are different.

13 In addition, the FSH beta subunit is specifically labeled with the N-term

14 no known mouse strains with mutations in the FSH beta gene.

15 n pathway, we produced mice deficient in the FSH beta subunit and therefore in FSH using ES cell tech

16 ated so far involving human mutations in the FSH beta, LH beta, or the gonadotropin receptor genes.

17 y genetically fusing the carboxyl end of the FSH beta subunit to the amino end of the alpha subunit i

18 1 amino acid loop between Y33 and F53 of the FSH beta-subunit (L2 beta) can be switched into L2 beta

19 The determinant loop of the FSH beta-subunit acts both as a specificity discriminato

20 ce within the receptor-binding domain of the FSH beta-subunit.

21 These contrasting results show that the FSH beta subunit is close to the N-terminal region and t

22 ICER binds to the FSH beta CRE site to reduce CREB occupation and abrogate

23 he tether, although covalently linked to the FSH beta domain, can functionally interact with a differ

24 cyclic AMP response element (CRE) within the FSH beta promoter resulted in the loss of preferential G

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