Djerid

el-Djerid, al-Jarīd (Arabic: الجريد‎; "Palm Leaf", Darija l-Jrīd) is a semidesert natural region comprising southern Tunisia and adjacent parts of Algeria and Libya.

Geography

The region is characterised by bare pink hills with oases and several chotts (salt pans) such as Chott el Djerid in Tunisia. Economically the area is important for phosphate mining. Major towns include Gafsa and Tozeur.

It remains the principal center of Ibāḍism in North Africa, with remaining Ibāḍī communities on Djerba in Tunisia, in the M'zab in Algeria, and in Jabal Nafusa in Libya. In medieval times, it often formed a politically separate entity under the control of Ibāḍī imams.

See also

References

External links

Media related to Djerid at Wikimedia Commons

Coordinates: 33°54′58″N 8°00′24″E / 33.91611°N 8.00667°E / 33.91611; 8.00667

JARID2

Protein Jumonji is a protein that in humans is encoded by the JARID2 gene.

Jarid2 (jumonji, AT rich interactive domain 2) is a protein coding gene that functions as a putative transcription factor. Distinguished as a nuclear protein necessary for mouse embryogenesis, Jarid2 is a member of the jumonji family that contains a DNA binding domain known as the AT-rich interaction domain (ARID)[2, 8, 11, 13]. In vitro studies of Jarid2 reveal that ARID along with other functional domains are involved in DNA binding, nuclear localization, transcriptional repression [5], and recruitment of Polycomb-repressive complex 2 (PRC2) [9, 10]. Intracellular mechanisms underlying these interactions remain largely unknown.

In search of developmentally important genes, Jarid2 has previously been identified by gene trap technology as an important factor necessary for organ development [2, 3, 5]. During mouse organogenesis, Jarid2 is involved in the formation of the neural tube and development of the liver, spleen, thymus and cardiovascular system [6, 12]. Continuous Jarid2 expression in the tissues of the heart, highlight its presiding role in the development of both the embryonic and the adult heart [2]. Mutant models of Jarid2 embryos show severe heart malformations, ventricular septal defects, noncompaction of the ventricular wall, and dilated atria [4]. Homozygous mutants of Jarid2 are found to die soon after birth [4]. Overexpression of the mouse Jarid2 gene has been reported to repress cardiomyocyte proliferation through it close interaction with retinoblastoma protein (Rb), a master cell cycle regulator [3, 5, 7]. Retinoblastoma-binding protein-2 and the human SMCX protein share regions of homology between mice and humans [1, 14].