| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-111 |
Sentence |
denotes |
Expression regulation and function of heparan sulfate 6-O-endosulfatases in the spermatogonial stem cell niche. |
| T1 |
0-111 |
Sentence |
denotes |
Expression regulation and function of heparan sulfate 6-O-endosulfatases in the spermatogonial stem cell niche. |
| TextSentencer_T2 |
112-204 |
Sentence |
denotes |
Glial cell line-derived neurotrophic factor (GDNF) is a heparan sulfate (HS)-binding factor. |
| T2 |
112-204 |
Sentence |
denotes |
Glial cell line-derived neurotrophic factor (GDNF) is a heparan sulfate (HS)-binding factor. |
| TextSentencer_T3 |
205-327 |
Sentence |
denotes |
GDNF is produced by somatic Sertoli cells, where it signals to maintain spermatogonial stem cells (SSCs) and reproduction. |
| T3 |
205-327 |
Sentence |
denotes |
GDNF is produced by somatic Sertoli cells, where it signals to maintain spermatogonial stem cells (SSCs) and reproduction. |
| TextSentencer_T4 |
328-486 |
Sentence |
denotes |
Here, we investigate the roles of extracellular HS 6-O-endosulfatases (Sulfs), Sulf1 and Sulf2, in the matrix transmission of GDNF from Sertoli cells to SSCs. |
| T4 |
328-486 |
Sentence |
denotes |
Here, we investigate the roles of extracellular HS 6-O-endosulfatases (Sulfs), Sulf1 and Sulf2, in the matrix transmission of GDNF from Sertoli cells to SSCs. |
| TextSentencer_T5 |
487-652 |
Sentence |
denotes |
Although Sulfs are not required for testis formation, Sulf deficiency leads to the accelerated depletion of SSCs, a testis phenotype similar to that of GDNF+/- mice. |
| T5 |
487-652 |
Sentence |
denotes |
Although Sulfs are not required for testis formation, Sulf deficiency leads to the accelerated depletion of SSCs, a testis phenotype similar to that of GDNF+/- mice. |
| TextSentencer_T6 |
653-735 |
Sentence |
denotes |
Mechanistically, we show that Sulfs are expressed in GDNF-producing Sertoli cells. |
| T6 |
653-735 |
Sentence |
denotes |
Mechanistically, we show that Sulfs are expressed in GDNF-producing Sertoli cells. |
| TextSentencer_T7 |
736-845 |
Sentence |
denotes |
In addition, reduced Sulf activity profoundly worsens haplo-deficient GDNF phenotypes in our genetic studies. |
| T7 |
736-845 |
Sentence |
denotes |
In addition, reduced Sulf activity profoundly worsens haplo-deficient GDNF phenotypes in our genetic studies. |
| TextSentencer_T8 |
846-1085 |
Sentence |
denotes |
These findings establish a critical role of Sulfs in promoting GDNF signaling and support a model in which Sulfs regulate the bioavailability of GDNF by enzymatically remodeling HS 6-O-desulfation to release GDNF from matrix sequestration. |
| T8 |
846-1085 |
Sentence |
denotes |
These findings establish a critical role of Sulfs in promoting GDNF signaling and support a model in which Sulfs regulate the bioavailability of GDNF by enzymatically remodeling HS 6-O-desulfation to release GDNF from matrix sequestration. |
| TextSentencer_T9 |
1086-1228 |
Sentence |
denotes |
Further, Sertoli cell-specific transcriptional factor Wilm's tumor 1 (WT1) directly activates the transcription of both Sulf1 and Sulf2 genes. |
| T9 |
1086-1228 |
Sentence |
denotes |
Further, Sertoli cell-specific transcriptional factor Wilm's tumor 1 (WT1) directly activates the transcription of both Sulf1 and Sulf2 genes. |
| TextSentencer_T10 |
1229-1444 |
Sentence |
denotes |
Together, our studies not only identify Sulfs as essential regulators of GDNF signaling in the SSC niche, but also as direct downstream targets of WT1, thus establishing a physiological role of WT1 in Sertoli cells. |
| T10 |
1229-1444 |
Sentence |
denotes |
Together, our studies not only identify Sulfs as essential regulators of GDNF signaling in the SSC niche, but also as direct downstream targets of WT1, thus establishing a physiological role of WT1 in Sertoli cells. |