Sema Domain, Immunoglobulin Domain (Ig), Transmembrane Domain (TM) and Short Cytoplasmic Domain, (Semaphorin) 4A Proteins (Sema4a)

Human Sema Domain, Immunoglobulin Domain (Ig), Transmembrane Domain (TM) and Short Cytoplasmic Domain, (Semaphorin) 4A (Sema4a) interaction partners

1. Human oligodendrocytes undergo apoptosis when exposed to Sema4A and take up H-ferritin for meeting iron requirements and that these functions are mediated via the Tim-1 (show ARHGEF5 Proteins) receptor. H-ferritin can block Sema4A-mediated cytotoxicity. Sema4A is detectable in the CSF (show CSF2 Proteins) of multiple sclerosis patients and HIV-seropositive persons and can induce oligodendrocyte cell death.

2. Advanced peri (show PLIN1 Proteins)-implantitis lesions showed higher levels of gene expression for Sem3A and Sem4D and lower levels of Sem4A in comparison to tissues obtained from a healthy dental implant.

3. Here we show three families with retinal degeneration in which unaffected family members are either homozygous or heterozygous for the variant. The p.R713Q variant in SEMA4A is insufficient to cause either autosomal recessive or autosomal dominant retinitis pigmentosa and is unlikely to be pathogenic.

4. ILT-4 (show LILRB2 Proteins) is a receptor for hSEMA4A)on activated CD4 (show CD4 Proteins)(+) T cells. hSEMA4A is highly expressed in human asthmatic lung tissue.

5. Suggest a role for Plexin-B1 (show PLXNB1 Proteins) as a ligand and Sema4A as a receptor and characterize a reverse signaling pathway downstream of Sema4A regulating cell migration via Scrib (show SCRIB Proteins).

6. SEMA (show SEMA3B Proteins) 4A confers doxorubicin resistance on hepatocellular carcinoma by inducing epithelialemesenchymal transition.

7. In this review, we summarized the current findings on neuroimmune Sema4A and Sema4D (show SEMA4D Proteins) molecules in chronic inflammation underlying many diseases and discussed their positive or negative impacts on the implicated molecular and cellular processes

8. Sema4A activated the Akt (show AKT1 Proteins) pathway via Plexin D1 (show PLXND1 Proteins) receptor in lung fibroblasts.Lung fibroblasts show elevated levels of Sema4A expression in systemic sclerosis patients.

9. Data suggest that increased expression of semaphorin 4A (Sema4A) is required to promote inflammation of rheumatoid arthritis (RA).

10. Germline variants in SEMA4A predispose to familial colorectal cancer type X.

Mouse (Murine) Sema Domain, Immunoglobulin Domain (Ig), Transmembrane Domain (TM) and Short Cytoplasmic Domain, (Semaphorin) 4A (Sema4a) interaction partners

1. Suggest a role for Plexin-B1 (show PLXNB1 Proteins) as a ligand and Sema4A as a receptor and characterize a reverse signaling pathway downstream of Sema4A regulating cell migration via Scrib (show SCRIB Proteins).

2. SEMA4A is required for optimal activation of mTORC1 in CD8 (show CD8A Proteins)+ T cells.

3. Treg-cell stability can be subverted in certain inflammatory sites, but is maintained by a Sema4a-Nrp1 (show NRP1 Proteins) axis-- this pathway is a potential therapeutic target that could limit Treg-cell-mediated tumour-induced tolerance without inducing autoimmunity

4. Data indicate that both semaphorin 4A mRNA and protein were clearly detected on the earliest progenitors and were downregulated through thymic development.

5. These results indicate the importance of the Sema4A protein conformation in human and mouse retina homeostasis.

6. A fraction of Sema4a-deficient transgenic BALB/c mice spontaneously develop skin lesions resembling atopic dermatitis (AD) in humans.

7. These data provide a new insight into Sema4A biology and define Sema4A as an important regulator of Th2-driven lung pathophysiology.

8. Sema4A activates a specialized and restricted genetic program in macrophages able to sustain angiogenesis and participates in their recruitment and activation in inflammatory injuries.

9. Sema4A regulates two distinct endosomal-sorting pathways that are critical for photoreceptor survival and phototransduction during the transition between daylight and darkness.

10. experiments using knockout mice revealed that Sema4A but not Sema7A (show SEMA7A Proteins) was required for the effect produced by Th1 (show HAND1 Proteins) cells on neurite outgrowth from cortical neurons.