KCNU1 Membrane Protein Introduction

Introduction of KCNU1

KCNU1, potassium channel subfamily U member 1, is a protein that in humans is encoded by the KCNU1 gene. It is also known as K_Ca5.1. The structure of this channel is related to the calcium-activated potassium channels, while it is activated by high intracellular pH and membrane voltage that mediates export of K⁺. KCNU1 is relatively insensitive to changes in calcium or magnesium concentrations. It may represent the primary spermatozoan K⁺ current.

Function of KCNU1 Membrane Protein

KCNU1 is a potassium channel which is also known as SLO3 or K_Ca5.1. KCNU1 channels are exclusively expressed in mammalian sperm, where variations of intracellular pH and membrane voltage are critical to cellular function through mediating export of potassium. In contrast to KCNMA1/SLO1, KCNU1 is not activated by Ca²⁺ or Mg²⁺. It has been reported that KCNU1 channel is critical for fertility. When faced with osmotic challenges, KCNU1 may play a critical role in sperm osmoregulation required for the acquisition of normal motility and morphology, especially those experienced after mixing with seminal fluid and entry into the vagina. In addition, KCNU1 channels have an effect on sperm progressive motility and morphology. This indicates that the mutations in KCNU1 and other channels may result in infertility. And KCNU1 variants can be induced by natural genetic variation. Furthermore, inhibition of KCNU1 by which quinine, quinidine and barium may alter sperm motility.

Fig.1 hSLO3 gating ring structure. (Leonetti, 2012)

Application of KCNU1 Membrane Protein in Literature

1. Zeng X.H., et al. Deletion of the Slo3 gene abolishes alkalization-activated K⁺ current in mouse spermatozoa. Proc Natl Acad Sci U S A. 2011, 108(14): 5879-84. PubMed ID: 21427226
   
   

   This article shows that KSper/Slo3 is the primary spermatozoan K(+) current, that KSper may play a critical role in the acquisition of normal morphology and sperm motility when faced with hyperosmotic challenges, and that Slo3 is critical for fertility.

2. Xia X.M., et al. Ligand-dependent activation of Slo family channels is defined by interchangeable cytosolic domains. J Neurosci. 2004, 24(24): 5585-91. PubMed ID: 15201331
   
   

   This article shows that Slo3 cytosolic module confers pH-dependent regulation on the Slo1 pore module, whereas the Slo1 cytosolic module confers Ca²⁺-dependent regulation on the Slo3 pore module. Therefore, ligand-specific regulation is defined by interchangeable cytosolic regulatory modules.

3. Geng Y., et al. A genetic variant of the sperm-specific SLO3 K⁺ channel has altered pH and Ca²⁺ sensitivities. J Biol Chem. 2017, 292(21): 8978-8987. PubMed ID: 28377504
   
   

   This study suggests that sperm-specific genes can evolve rapidly and natural genetic variation may lead to a SLO3 variant that differs from wild type in both pH and intracellular Ca²⁺ sensitivities. Whether this physiological variation confers differences in fertility among males remains to be established.

4. Carkci S., et al. Ion channel gene expressions in infertile men: A case-control study. Int J Reprod Biomed (Yazd). 2017, 15(12): 749-756. PubMed ID: 29492471
   
   

   This article reveals that KCNU1 channels have an effect on sperm progressive motility and morphology. This indicates that the mutations in KCNU1 and other channels may result in infertility.

5. Wrighton D.C., et al. Mechanism of inhibition of mouse Slo3 (KCa 5.1) potassium channels by quinine, quinidine, and barium. Br J Pharmacol. 2015,172(17): 4355-63. PubMed ID: 26045093
   
   

   This article investigates the mechanism by which quinine, quinidine, and barium inhibit Slo3 channels.

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Reference

1. Leonetti M D, et al. (2012). Functional and structural analysis of the human SLO3 pH- and voltage-gated K⁺ channel. Proc Natl Acad Sci U S A. 109(47): 19274-9.

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