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Gene Review

PRM3  -  protamine 3

Homo sapiens

Synonyms: Protamine-3, Sperm protamine P3
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Disease relevance of PRM3

  • Hence, the ability of Prm3 and a series of Prm3 deleted/mutated subfragments to direct reporter gene expression in human erythroleukemia 92.1.7 and human embryonic kidney 293 cells was investigated [1].

High impact information on PRM3

  • Previous studies established that 15d-Delta12,14-prostaglandin J2 (15d-PGJ2) selectively inhibits Prm3 activity and TPbeta expression through a peroxisome proliferator-activated receptor (PPAR)gamma mechanism without affecting Prm1 activity or TPalpha expression in human megakaryocytic erythroleukemia (HEL) 92.1.7 cells [2].
  • Furthermore, the binary (activator) complex formed between PG and SAK mutant, PRM3, lacking the N-terminal lysine 11, exhibited 3-4-fold reduced binding with PG, Pm or miniplasmin substrate during ternary complex formation as compared to native SAK [3].
  • The results show that human protamine 3 elutes first, closely followed by protamine 2 [4].
  • The aim of the current study was to determine the key factors regulating TPbeta expression by functionally characterizing Prm3, identifying the core promoter and the cis-acting elements regulating basal Prm3 activity [1].
  • Moreover, herein it was established that the core AP-1 element mediates phorbol myristic acid-induction of Prm3 activity hence providing a mechanistic explanation of phorbol ester up-regulation of TPbeta mRNA expression [1].

Biological context of PRM3

  • Furthermore, three distinct regulatory regions comprising of an upstream repressor sequence, located between -404 to -320, and two positive regulatory regions required for efficient basal gene expression, located between -154 to -106 and -50 to +1, were identified within the core Prm3 [1].

Anatomical context of PRM3


Other interactions of PRM3

  • Analysis described here supports the view that a fourth candidate coding region, gene4/Prm3, was derived from PRM1 during the genesis of the PRM1-->PRM2-->TNP2 domain [6].

Analytical, diagnostic and therapeutic context of PRM3

  • Deletion and site-directed mutagenesis of consensus Oct-1/2 and AP-1 elements within the latter -154 to -106 and -50 to +1 regions, respectively, substantially reduced Prm3 activity while mutation of both elements abolished Prm3 activity [1].


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