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Gene Review

GEMIN2  -  gem (nuclear organelle) associated protein 2

Homo sapiens

Synonyms: Component of gems 2, Gem-associated protein 2, Gemin-2, SIP1, SIP1-delta, ...
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Disease relevance of SIP1


Psychiatry related information on SIP1


High impact information on SIP1


Chemical compound and disease context of SIP1


Biological context of SIP1

  • Survival motor neuron (SMN) interacting protein 1 (SIP1) interacts with SMN protein and plays a crucial role in the biogenesis of spliceosomes [2].
  • Next, we determined the exon-intron structure of the SIP1 gene which encompasses 10 exons and identified five transcription isoforms [4].
  • These findings suggest that an aberrant alternative splicing event in SIP1 occurs tissues derived from patients with the motor neuron diseases, and contributes to the pathological process of SMA and ALS [2].
  • SIP1/ZEB2 is a member of the deltaEF-1 family of two-handed zinc finger nuclear factors [3].
  • Here, we show that expression of SIP1 in human epithelial cells results in a clear morphological change from an epithelial to a mesenchymal phenotype [3].

Anatomical context of SIP1


Associations of SIP1 with chemical compounds

  • Finally, treatment of cells with leptomycin B (a drug that blocks export of U snRNAs to the cytoplasm and consequently import of new snRNPs into the nucleus) is shown to deplete snRNPs (but not SMN or SIP1) from the Cajal body [11].

Physical interactions of SIP1


Other interactions of SIP1


Analytical, diagnostic and therapeutic context of SIP1

  • The presence of SMN and SIP1 in Cajal bodies is confirmed by immunoelectron microscopy and by microinjection of antibodies that interfere with the integrity of the structure [11].
  • ELISA detected IgG specific to Sip1 C-ter in sera from 11/56 (20%) patients with Behçet's disease, IgM in 23/56 (41%) and IgA in 9/54 (17%) [17].


  1. Nonsense and frameshift mutations in ZFHX1B, encoding Smad-interacting protein 1, cause a complex developmental disorder with a great variety of clinical features. Yamada, K., Yamada, Y., Nomura, N., Miura, K., Wakako, R., Hayakawa, C., Matsumoto, A., Kumagai, T., Yoshimura, I., Miyazaki, S., Kato, K., Sonta, S., Ono, H., Yamanaka, T., Nagaya, M., Wakamatsu, N. Am. J. Hum. Genet. (2001) [Pubmed]
  2. Increased expression level of the splicing variant of SIP1 in motor neuron diseases. Aerbajinai, W., Ishihara, T., Arahata, K., Tsukahara, T. Int. J. Biochem. Cell Biol. (2002) [Pubmed]
  3. SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell-cell junctions. Vandewalle, C., Comijn, J., De Craene, B., Vermassen, P., Bruyneel, E., Andersen, H., Tulchinsky, E., Van Roy, F., Berx, G. Nucleic Acids Res. (2005) [Pubmed]
  4. An essential SMN interacting protein (SIP1) is not involved in the phenotypic variability of spinal muscular atrophy (SMA). Helmken, C., Wetter, A., Rudnik-Schöneborn, S., Liehr, T., Zerres, K., Wirth, B. Eur. J. Hum. Genet. (2000) [Pubmed]
  5. The two-handed E box binding zinc finger protein SIP1 downregulates E-cadherin and induces invasion. Comijn, J., Berx, G., Vermassen, P., Verschueren, K., van Grunsven, L., Bruyneel, E., Mareel, M., Huylebroeck, D., van Roy, F. Mol. Cell (2001) [Pubmed]
  6. "Mowat-Wilson" syndrome with and without Hirschsprung disease is a distinct, recognizable multiple congenital anomalies-mental retardation syndrome caused by mutations in the zinc finger homeo box 1B gene. Zweier, C., Albrecht, B., Mitulla, B., Behrens, R., Beese, M., Gillessen-Kaesbach, G., Rott, H.D., Rauch, A. Am. J. Med. Genet. (2002) [Pubmed]
  7. Mutations in SIP1, encoding Smad interacting protein-1, cause a form of Hirschsprung disease. Wakamatsu, N., Yamada, Y., Yamada, K., Ono, T., Nomura, N., Taniguchi, H., Kitoh, H., Mutoh, N., Yamanaka, T., Mushiake, K., Kato, K., Sonta , S., Nagaya, M. Nat. Genet. (2001) [Pubmed]
  8. The spinal muscular atrophy disease gene product, SMN, and its associated protein SIP1 are in a complex with spliceosomal snRNP proteins. Liu, Q., Fischer, U., Wang, F., Dreyfuss, G. Cell (1997) [Pubmed]
  9. The SMN-SIP1 complex has an essential role in spliceosomal snRNP biogenesis. Fischer, U., Liu, Q., Dreyfuss, G. Cell (1997) [Pubmed]
  10. Differential expression of the epithelial-mesenchymal transition regulators snail, SIP1, and twist in gastric cancer. Rosivatz, E., Becker, I., Specht, K., Fricke, E., Luber, B., Busch, R., Höfler, H., Becker, K.F. Am. J. Pathol. (2002) [Pubmed]
  11. The spinal muscular atrophy disease gene product, SMN: A link between snRNP biogenesis and the Cajal (coiled) body. Carvalho, T., Almeida, F., Calapez, A., Lafarga, M., Berciano, M.T., Carmo-Fonseca, M. J. Cell Biol. (1999) [Pubmed]
  12. Multiprotein complexes of the survival of motor neuron protein SMN with Gemins traffic to neuronal processes and growth cones of motor neurons. Zhang, H., Xing, L., Rossoll, W., Wichterle, H., Singer, R.H., Bassell, G.J. J. Neurosci. (2006) [Pubmed]
  13. Gemin4. A novel component of the SMN complex that is found in both gems and nucleoli. Charroux, B., Pellizzoni, L., Perkinson, R.A., Yong, J., Shevchenko, A., Mann, M., Dreyfuss, G. J. Cell Biol. (2000) [Pubmed]
  14. Gemin5, a novel WD repeat protein component of the SMN complex that binds Sm proteins. Gubitz, A.K., Mourelatos, Z., Abel, L., Rappsilber, J., Mann, M., Dreyfuss, G. J. Biol. Chem. (2002) [Pubmed]
  15. The SMN complex is associated with snRNPs throughout their cytoplasmic assembly pathway. Massenet, S., Pellizzoni, L., Paushkin, S., Mattaj, I.W., Dreyfuss, G. Mol. Cell. Biol. (2002) [Pubmed]
  16. Identification of a novel human immunodeficiency virus type 1 integrase interactor, Gemin2, that facilitates efficient viral cDNA synthesis in vivo. Hamamoto, S., Nishitsuji, H., Amagasa, T., Kannagi, M., Masuda, T. J. Virol. (2006) [Pubmed]
  17. Identification and characterization of the carboxy-terminal region of Sip-1, a novel autoantigen in Behçet's disease. Delunardo, F., Conti, F., Margutti, P., Alessandri, C., Priori, R., Siracusano, A., Riganò, R., Profumo, E., Valesini, G., Sorice, M., Ortona, E. Arthritis Res. Ther. (2006) [Pubmed]
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