MAPK8

MAPK8
MAP quinasa 8
Protein MAPK8 PDB 1jnk.png
Estructura tridimensional de la proteína MAPK8.
HUGO 6881
Símbolo MAPK8
Símbolos alt. JNK, JNK1, JNK1A2, JNK21B1/2, PRKM8, SAPK1
Datos genéticos
Locus Cr. 10 q11.22
Bases de datos
Entrez 5599
OMIM 601158
PDB 1jnk
RefSeq NP_002741
UniProt P45983

La MAP quinasa 8 (MAPK8) es una enzima codificada en humanos por el gen mapk8.[1] [2]

La MAPK8 pertenece a la familia de las MAP quinasas. Las MAP quinasas actúan como punto de integración de múltiples señales bioquímicas, y están implicadas en una amplia variedad de procesos celulares tales como proliferación celular, diferenciación celular, regulación de la transcripción y desarrollo. La MAPK8 es activada por diversos estímulos celulares y factores de transcripción específicos, actuando como mediador de la expresión génica inmediata en respuesta a determinados estímulos. La activación de esta quinasa por el factor de necrosis tumoral alfa (TNF-α) parece ser necesaria en el proceso de apoptosis inducida por TNF-α. La MAPK8 también está implicada en la apoptosis inducida por radiación UV, que se piensa que está relacionada con la ruta de muerte celular mediada por citocromo c. Estudios de este gen llevados a cabo en ratones sugieren que esta quinasa juega un papel clave en la proliferación, diferenciación y apoptosis de linfocitos T. Se han descrito cuatro variantes transcripcionales de este gen, que codifican diversas isoformas de la quinasa.[3]

Interacciones

La proteína MAPK8 ha demostrado ser capaz de interaccionar con:

Véase también

  • MAP quinasas (MAPK)

Referencias

  1. ↑ a b Derijard B, Hibi M, Wu IH, Barrett T, Su B, Deng T, Karin M, Davis RJ (Apr 1994). «JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain». Cell 76 (6):  pp. 1025–37. PMID 8137421. 
  2. ↑ Gupta S, Barrett T, Whitmarsh AJ, Cavanagh J, Sluss HK, Derijard B, Davis RJ (Jul 1996). «Selective interaction of JNK protein kinase isoforms with transcription factors». EMBO J 15 (11):  pp. 2760–70. PMID 8654373. 
  3. ↑ «Entrez Gene: MAPK8 mitogen-activated protein kinase 8».
  4. ↑ Mao, C; Ray-Gallet D, Tavitian A, Moreau-Gachelin F (Feb. 1996). «Differential phosphorylations of Spi-B and Spi-1 transcription factors». Oncogene (ENGLAND) 12 (4):  pp. 863–73. ISSN 0950-9232. PMID 8632909. 
  5. ↑ Slack, D N; Seternes O M, Gabrielsen M, Keyse S M (May. 2001). «Distinct binding determinants for ERK2/p38alpha and JNK map kinases mediate catalytic activation and substrate selectivity of map kinase phosphatase-1». J. Biol. Chem. (United States) 276 (19):  pp. 16491–500. doi:10.1074/jbc.M010966200. ISSN 0021-9258. PMID 11278799. 
  6. ↑ Raingeaud, J; Gupta S, Rogers J S, Dickens M, Han J, Ulevitch R J, Davis R J (Mar. 1995). «Pro-inflammatory cytokines and environmental stress cause p38 mitogen-activated protein kinase activation by dual phosphorylation on tyrosine and threonine». J. Biol. Chem. (UNITED STATES) 270 (13):  pp. 7420–6. ISSN 0021-9258. PMID 7535770. 
  7. ↑ Fuchs, S Y; Xie B, Adler V, Fried V A, Davis R J, Ronai Z (Dec. 1997). «c-Jun NH2-terminal kinases target the ubiquitination of their associated transcription factors». J. Biol. Chem. (UNITED STATES) 272 (51):  pp. 32163–8. ISSN 0021-9258. PMID 9405416. 
  8. ↑ a b Chen, Z; Cobb M H (May. 2001). «Regulation of stress-responsive mitogen-activated protein (MAP) kinase pathways by TAO2». J. Biol. Chem. (United States) 276 (19):  pp. 16070–5. doi:10.1074/jbc.M100681200. ISSN 0021-9258. PMID 11279118. 
  9. ↑ a b c d Tournier, C; Whitmarsh A J, Cavanagh J, Barrett T, Davis R J (Jul. 1997). «Mitogen-activated protein kinase kinase 7 is an activator of the c-Jun NH2-terminal kinase». Proc. Natl. Acad. Sci. U.S.A. (UNITED STATES) 94 (14):  pp. 7337–42. ISSN 0027-8424. PMID 9207092. 
  10. ↑ Wiltshire, Carolyn; Matsushita Masato, Tsukada Satoshi, Gillespie David A F, May Gerhard H W (Nov. 2002). «A new c-Jun N-terminal kinase (JNK)-interacting protein, Sab (SH3BP5), associates with mitochondria». Biochem. J. (England) 367 (Pt 3):  pp. 577–85. doi:10.1042/BJ20020553. ISSN 0264-6021. PMID 12167088. 
  11. ↑ Wang, T; Arifoglu P, Ronai Z, Tew K D (Jun. 2001). «Glutathione S-transferase P1-1 (GSTP1-1) inhibits c-Jun N-terminal kinase (JNK1) signaling through interaction with the C terminus». J. Biol. Chem. (United States) 276 (24):  pp. 20999–1003. doi:10.1074/jbc.M101355200. ISSN 0021-9258. PMID 11279197. 
  12. ↑ Whitmarsh, A J; Cavanagh J, Tournier C, Yasuda J, Davis R J (Sep. 1998). «A mammalian scaffold complex that selectively mediates MAP kinase activation». Science (UNITED STATES) 281 (5383):  pp. 1671–4. ISSN 0036-8075. PMID 9767029. 
  13. ↑ Cai, Yi; Lechner Mark S, Nihalani Deepak, Prindle Marc J, Holzman Lawrence B, Dressler Gregory R (Jan. 2002). «Phosphorylation of Pax2 by the c-Jun N-terminal kinase and enhanced Pax2-dependent transcription activation». J. Biol. Chem. (United States) 277 (2):  pp. 1217–22. doi:10.1074/jbc.M109663200. ISSN 0021-9258. PMID 11700324. 
  14. ↑ a b c Cheng, J; Yang J, Xia Y, Karin M, Su B (Apr. 2000). «Synergistic interaction of MEK kinase 2, c-Jun N-terminal kinase (JNK) kinase 2, and JNK1 results in efficient and specific JNK1 activation». Mol. Cell. Biol. (UNITED STATES) 20 (7):  pp. 2334–42. ISSN 0270-7306. PMID 10713157. 
  15. ↑ Girardin, S E; Yaniv M (Jul. 2001). «A direct interaction between JNK1 and CrkII is critical for Rac1-induced JNK activation». EMBO J. (England) 20 (13):  pp. 3437–46. doi:10.1093/emboj/20.13.3437. ISSN 0261-4189. PMID 11432831. 
  16. ↑ Lee, Clement M; Onésime Djamila, Reddy C Damodara, Dhanasekaran N, Reddy E Premkumar (Oct. 2002). «JLP: A scaffolding protein that tethers JNK/p38MAPK signaling modules and transcription factors». Proc. Natl. Acad. Sci. U.S.A. (United States) 99 (22):  pp. 14189–94. doi:10.1073/pnas.232310199. ISSN 0027-8424. PMID 12391307. 
  17. ↑ Park, Hee-Sae; Kim Mi-Sung, Huh Sung-Ho, Park Jihyun, Chung Jongkyeong, Kang Sang Sun, Choi Eui-Ju (Jan. 2002). «Akt (protein kinase B) negatively regulates SEK1 by means of protein phosphorylation». J. Biol. Chem. (United States) 277 (4):  pp. 2573–8. doi:10.1074/jbc.M110299200. ISSN 0021-9258. PMID 11707464. 
  18. ↑ Aoyama, K; Nagata M, Oshima K, Matsuda T, Aoki N (Jul. 2001). «Molecular cloning and characterization of a novel dual specificity phosphatase, LMW-DSP2, that lacks the cdc25 homology domain». J. Biol. Chem. (United States) 276 (29):  pp. 27575–83. doi:10.1074/jbc.M100408200. ISSN 0021-9258. PMID 11346645. 
  19. ↑ Noguchi, K; Kitanaka C, Yamana H, Kokubu A, Mochizuki T, Kuchino Y (Nov. 1999). «Regulation of c-Myc through phosphorylation at Ser-62 and Ser-71 by c-Jun N-terminal kinase». J. Biol. Chem. (UNITED STATES) 274 (46):  pp. 32580–7. ISSN 0021-9258. PMID 10551811. 
  20. ↑ Tanoue, T; Moriguchi T, Nishida E (Jul. 1999). «Molecular cloning and characterization of a novel dual specificity phosphatase, MKP-5». J. Biol. Chem. (UNITED STATES) 274 (28):  pp. 19949–56. ISSN 0021-9258. PMID 10391943. 
  21. ↑ a b Meyer, C F; Wang X, Chang C, Templeton D, Tan T H (Apr. 1996). «Interaction between c-Rel and the mitogen-activated protein kinase kinase kinase 1 signaling cascade in mediating kappaB enhancer activation». J. Biol. Chem. (UNITED STATES) 271 (15):  pp. 8971–6. ISSN 0021-9258. PMID 8621542. 
  22. ↑ Ito, M; Yoshioka K, Akechi M, Yamashita S, Takamatsu N, Sugiyama K, Hibi M, Nakabeppu Y, Shiba T, Yamamoto K I (Nov. 1999). «JSAP1, a novel jun N-terminal protein kinase (JNK)-binding protein that functions as a Scaffold factor in the JNK signaling pathway». Mol. Cell. Biol. (UNITED STATES) 19 (11):  pp. 7539–48. ISSN 0270-7306. PMID 10523642. 
  23. ↑ Kelkar, N; Gupta S, Dickens M, Davis R J (Feb. 2000). «Interaction of a mitogen-activated protein kinase signaling module with the neuronal protein JIP3». Mol. Cell. Biol. (UNITED STATES) 20 (3):  pp. 1030–43. ISSN 0270-7306. PMID 10629060. 
  24. ↑ Aguirre, Vincent; Werner Eric D, Giraud Jodel, Lee Yong Hee, Shoelson Steve E, White Morris F (Jan. 2002). «Phosphorylation of Ser307 in insulin receptor substrate-1 blocks interactions with the insulin receptor and inhibits insulin action». J. Biol. Chem. (United States) 277 (2):  pp. 1531–7. doi:10.1074/jbc.M101521200. ISSN 0021-9258. PMID 11606564. 
  25. ↑ Aguirre, V; Uchida T, Yenush L, Davis R, White M F (Mar. 2000). «The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307)». J. Biol. Chem. (UNITED STATES) 275 (12):  pp. 9047–54. ISSN 0021-9258. PMID 10722755. 
  26. ↑ Xu, S; Cobb M H (Dec. 1997). «MEKK1 binds directly to the c-Jun N-terminal kinases/stress-activated protein kinases». J. Biol. Chem. (UNITED STATES) 272 (51):  pp. 32056–60. ISSN 0021-9258. PMID 9405400. 
  27. ↑ Ishitani, Tohru; Takaesu Giichi, Ninomiya-Tsuji Jun, Shibuya Hiroshi, Gaynor Richard B, Matsumoto Kunihiro (Dec. 2003). «Role of the TAB2-related protein TAB3 in IL-1 and TNF signaling». EMBO J. (England) 22 (23):  pp. 6277–88. doi:10.1093/emboj/cdg605. ISSN 0261-4189. PMID 14633987. 
  28. ↑ Nishitoh, H; Saitoh M, Mochida Y, Takeda K, Nakano H, Rothe M, Miyazono K, Ichijo H (Sep. 1998). «ASK1 is essential for JNK/SAPK activation by TRAF2». Mol. Cell (UNITED STATES) 2 (3):  pp. 389–95. ISSN 1097-2765. PMID 9774977. 
  29. ↑ Yazgan, Oya; Pfarr Curt M (Aug. 2002). «Regulation of two JunD isoforms by Jun N-terminal kinases». J. Biol. Chem. (United States) 277 (33):  pp. 29710–8. doi:10.1074/jbc.M204552200. ISSN 0021-9258. PMID 12052834. 
  30. ↑ Tada, K; Okazaki T, Sakon S, Kobarai T, Kurosawa K, Yamaoka S, Hashimoto H, Mak T W, Yagita H, Okumura K, Yeh W C, Nakano H (Sep. 2001). «Critical roles of TRAF2 and TRAF5 in tumor necrosis factor-induced NF-kappa B activation and protection from cell death». J. Biol. Chem. (United States) 276 (39):  pp. 36530–4. doi:10.1074/jbc.M104837200. ISSN 0021-9258. PMID 11479302. 
  31. ↑ Cano, E; Hazzalin C A, Kardalinou E, Buckle R S, Mahadevan L C (Nov. 1995). «Neither ERK nor JNK/SAPK MAP kinase subtypes are essential for histone H3/HMG-14 phosphorylation or c-fos and c-jun induction». J. Cell. Sci. (ENGLAND) 108 ( Pt 11):  pp. 3599–609. ISSN 0021-9533. PMID 8586671. 

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