High impact information on Hhat

• Our molecular analysis of knockout mice deficient in Skn, the murine homolog of the Drosophila ski gene, which catalyzes Hh palmitoylation, and gene-targeted mice producing a nonpalmitoylated form of Shh indicates that Hh palmitoylation is essential for its activity as well as the generation of a protein gradient in the developing embryos [1].
• Adoptive transfer of skin-selective autoimmunity induced by Skn alloantigenic disparities [2].
• Normally compatible A strain skin grafts, but not Skn-compatible B6 skin grafts, were rejected by cyclophosphamide-treated (B6 x A)F1 recipients of (B6 x A)/B6 spleen cells from Skn-primed chimera donors [2].
• The role of IL-7 was further supported in that mice cotransferred with Skn-immune cells plus normal spleen cells, but also treated with anti-IL-7 Ab, no longer exhibited reduced lesion severity [3].
• A comparison has been made of the abilities of bone marrow cells and lymph node cells to induce tolerance of skin when inoculated into neonatal rats known to differ only with regard to non-MHC incompatibilities, including putative skin-specific (Skn) antigens [4].

Biological context of Hhat

• An immunogenetic analysis Skn antigens in mice [5].
• Skin graft rejection in mice repopulated with marrow of the skin donor type: a Skn gene in a congenic line [6].

Anatomical context of Hhat

• Our studies were designed primarily to test the inference that (B6 x A)F1 lymphoid cells, after differentiating in B6 recipients, which lack the Skn alloantigens of A strain mice, may make an Skn-related, skin-selective autoimmune response when returned to their native (B6 x A)F1 habitat [2].
• In a murine model of autoimmunity targeted against the epidermal cell Ags, Skn, adoptive transfer of Skn-immune T cells to immunosuppressed recipients elicits skin lesions in areas of mild epidermal trauma [3].

Associations of Hhat with chemical compounds

• IL-7 is a critical factor in modulating lesion development in Skn-directed autoimmunity [3].

Analytical, diagnostic and therapeutic context of Hhat

• Spleen cells of control female chimeras primed by grafting and rejection of H-Y (Skn-compatible) B6 male skin failed to incite the Skn-typical cutaneous lesions in (B6 x A)F1 recipients, indicating that these lesions were Skn-specific and not a nonspecific consequence of incompatible skin grafting per se [2].
• Demonstration of Skn antigens on mouse epidermal cells by immunofluorescence and flow cytometry [7].

References