Junctophilins: A novel family of junctional membrane complex proteins

被引:541
作者
Takeshima, H [1 ]
Komazaki, S
Nishi, M
Lino, M
Kangawa, K
机构
[1] Kurume Univ, Div Cell Biol, Inst Life Sci, Kurume, Fukuoka 8390861, Japan
[2] Univ Tokyo, Fac Med, Dept Pharmacol, Bunkyo Ku, Tokyo 1138654, Japan
[3] Japan Sci & Technol Corp, CREST, Bunkyo Ku, Tokyo 1138654, Japan
[4] Saitama Med Sch, Dept Anat, Moroyama, Saitama 3500495, Japan
[5] Natl Cardiovasc Ctr, Res Inst, Dept Biochem, Suita, Osaka 5658565, Japan
关键词
D O I
10.1016/S1097-2765(00)00003-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Junctional complexes between the plasma membrane (PM) and endoplasmic/sarcoplasmic reticulum (ER/SR) are a common feature of all excitable cell types and mediate cross-talk between cell surface and intracellular ion channels. We have identified the junctophilins (JPs), a novel conserved family of proteins that are components of the junctional complexes. JPs are composed of a carboxy-terminal hydrophobic segment spanning the ER/SR membrane and a remaining cytoplasmic domain that shows specific affinity for the PM. In mouse, there are at least three JP subtypes: JP-1, -2, and -3. JP-2 is abundantly expressed in the heart, and mutant mice lacking JP-2 exhibited embryonic lethality. Cardiac myocytes from the mutant mice showed deficiency of the junctional membrane complexes and abnormal Ca2+ transients. Our results suggest that JPs are important components of junctional membrane complexes.
引用
收藏
页码:11 / 22
页数:12
相关论文
共 31 条
[1]   CELLULAR-ORIGINS OF THE TRANSIENT INWARD CURRENT IN CARDIAC MYOCYTES - ROLE OF FLUCTUATIONS AND WAVES OF ELEVATED INTRACELLULAR CALCIUM [J].
BERLIN, JR ;
CANNELL, MB ;
LEDERER, WJ .
CIRCULATION RESEARCH, 1989, 65 (01) :115-126
[2]   Neuronal calcium signaling [J].
Berridge, MJ .
NEURON, 1998, 21 (01) :13-26
[3]   Sparks of interest in cardiac excitation-contraction coupling [J].
Cannell, MB ;
Soeller, C .
TRENDS IN PHARMACOLOGICAL SCIENCES, 1998, 19 (01) :16-20
[4]  
Fabiato A, 1978, Ann N Y Acad Sci, V307, P491, DOI 10.1111/j.1749-6632.1978.tb41979.x
[5]   DISULFIDE BONDS, N-GLYCOSYLATION AND TRANSMEMBRANE TOPOLOGY OF SKELETAL-MUSCLE TRIADIN [J].
FAN, HR ;
BRANDT, NR ;
CASWELL, AH .
BIOCHEMISTRY, 1995, 34 (45) :14902-14908
[6]   ULTRASTRUCTURE OF CAT MYOCARDIUM .I. VENTRICULAR PAPILLARY MUSCLE [J].
FAWCETT, DW ;
MCNUTT, NS .
JOURNAL OF CELL BIOLOGY, 1969, 42 (01) :1-&
[7]   RECENT INSIGHTS INTO THE REGULATION OF CARDIAC CA2+ FLUX DURING PERINATAL-DEVELOPMENT AND IN CARDIAC-FAILURE [J].
FISHER, DJ .
CURRENT OPINION IN CARDIOLOGY, 1995, 10 (01) :44-51
[8]   STRUCTURAL-ANALYSIS OF MUSCLE DEVELOPMENT - TRANSVERSE TUBULES, SARCOPLASMIC-RETICULUM, AND THE TRIAD [J].
FLUCHER, BE .
DEVELOPMENTAL BIOLOGY, 1992, 154 (02) :245-260
[9]   MUSCLE-FIBERS FROM DYSGENIC MOUSE INVIVO LACK A SURFACE COMPONENT OF PERIPHERAL COUPLINGS [J].
FRANZINIARMSTRONG, C ;
PINCONRAYMOND, M ;
RIEGER, F .
DEVELOPMENTAL BIOLOGY, 1991, 146 (02) :364-376
[10]   Functional and morphological features of skeletal muscle from mutant mice lacking both type 1 And type 3 ryanodine receptors [J].
Ikemoto, T ;
Komazaki, S ;
Takeshima, H ;
Nishi, M ;
Noda, T ;
Iino, M ;
Endo, M .
JOURNAL OF PHYSIOLOGY-LONDON, 1997, 501 (02) :305-312