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10.1530/JME-12-0219 http://scihub22266oqcxt.onion/10.1530/JME-12-0219 C4404413!4404413 !23511952     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\23511952 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Mol+Endocrinol 2013 ; 50 (3 ): 375-87 Nephropedia Template TP {{tp|p=23511952 |t=2013. Thyroid-specific inactivation of KIF3A alters the TSH signaling pathway and leads to hypothyroidism |pdf=|usr=}}{{23511952 }} gab.com Text Thyroid-specific inactivation of KIF3A alters the TSH signaling pathway and leads to hypothyroidism JO: J Mol Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=23511952 #FOAvip Kinesins, including the kinesin 2/KIF3 molecular motor, play an important role in intracellular traffic and can deliver vesicles to distal axon terminals, to cilia, to nonpolarized cell surfaces or to epithelial cell basolateral membranes, thus taking part in the establishment of cellular polarity. We report here the consequences of kinesin 2 motor inactivation in the thyroid of 3-week-old Kif3a(?)(/flox) Pax8(Cre/)(+) mutant mice. Our results indicate first that 3-week-old Pax8(Cre/)(+) mice used in these experiments present minor thyroid functional defects resulting in a slight increase in circulating bioactive TSH and intracellular cAMP levels, sufficient to maintain blood thyroxine levels in the normal range. Second, Kif3a inactivation in thyrocytes markedly amplified the phenotype observed in Pax8(Cre/)(+) mice, resulting in altered TSH signaling upstream of the second messenger cAMP and mild hypothyroidism. Finally, our results in mouse embryonic fibroblasts indicate that Kif3a inactivation in the absence of any Pax8 gene alteration leads to altered G protein-coupled receptor plasma membrane expression, as shown for the ?2 adrenergic receptor, and we suggest that a similar mechanism may explain the altered TSH signaling and mild hypothyroidism detected in Kif3a(?)(/flox) Pax8(Cre/)(+) mutant mice. Twit Text FOAVip Thyroid-specific inactivation of KIF3A alters the TSH signaling pathway and leads to hypothyroidism ????J Mol Endocrinol http://www.kidney.de/pget.php?&tw=1&pmid=23511952 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23511952 #FOAvip English Wikipedia <ref>{{Cite pmid|23511952 }}</ref> Thyroid-specific inactivation of KIF3A alters the TSH signaling pathway and leads to hypothyroidism #MMPMID23511952 D'Amico E ; Gayral S ; Massart C ; Van Sande J ; Reiter JF ; Dumont JE ; Robaye B ; Schurmans S J Mol Endocrinol 2013[Jun]; 50 (3 ): 375-87 PMID23511952 show ga Kinesins, including the kinesin 2/KIF3 molecular motor, play an important role in intracellular traffic and can deliver vesicles to distal axon terminals, to cilia, to nonpolarized cell surfaces or to epithelial cell basolateral membranes, thus taking part in the establishment of cellular polarity. We report here the consequences of kinesin 2 motor inactivation in the thyroid of 3-week-old Kif3a(?)(/flox) Pax8(Cre/)(+) mutant mice. Our results indicate first that 3-week-old Pax8(Cre/)(+) mice used in these experiments present minor thyroid functional defects resulting in a slight increase in circulating bioactive TSH and intracellular cAMP levels, sufficient to maintain blood thyroxine levels in the normal range. Second, Kif3a inactivation in thyrocytes markedly amplified the phenotype observed in Pax8(Cre/)(+) mice, resulting in altered TSH signaling upstream of the second messenger cAMP and mild hypothyroidism. Finally, our results in mouse embryonic fibroblasts indicate that Kif3a inactivation in the absence of any Pax8 gene alteration leads to altered G protein-coupled receptor plasma membrane expression, as shown for the ?2 adrenergic receptor, and we suggest that a similar mechanism may explain the altered TSH signaling and mild hypothyroidism detected in Kif3a(?)(/flox) Pax8(Cre/)(+) mutant mice. |Animals [MESH] |Hypothyroidism/*etiology/*metabolism [MESH] |Kinesins/genetics/*metabolism [MESH] |Mice [MESH] |Mice, Mutant Strains [MESH] |PAX8 Transcription Factor [MESH] |Paired Box Transcription Factors/genetics/metabolism [MESH] |Signal Transduction/genetics/physiology [MESH] |Thyroid Gland/*metabolism [MESH]Thyroid-specific inactivation of KIF3A alters the TSH signaling pathwa(epmc).pdf DeepDyve Pubget Overpricing