heptad repeat 1-heptad repeat 2 region (ectodomain) of the transmembrane subunit of human T-cell leukemia virus type 1 (HTLV-1), and related domains; This domain subfamily spans both heptad repeats of the glycoprotein (gp)/transmembrane(TM) subunit of various endogenous retroviruses (ERVs) and infectious retroviruses, including HTLV-1, HTLV -2, primate Mason-Pfizer monkey virus, Moloney murine leukemia virus, simian T-cell lymphotropic virus, feline leukemia virus (FeLV), bovine leukemia virus, and various human endogenous retroviruses (HERVs), including, HERV-H1_c2q24.3, HERV-H2_3q26, HERV-F(c)1_cXq21.33, HERV-T_19q13.11, Syncytin-1 (HERV-W_c7q21.2/ ERVWE1), Syncytin-2 (HERV-FRD_6p24.1), and related domains. This domain includes an N-terminal heptad repeat, a CKS17-like immunosuppressive region, a CX6C motif that forms an intrasubunit disulfide bond, and a C-terminal heptad repeat. N-terminal to HR1-HR2 region is a fusion peptide (FP), and C-terminal, is a membrane-spanning region (MSR). Viral infection involves the formation of a trimer-of-hairpins structure (three HR1s helices, buttressed by three HR2 helices lying in antiparallel orientation). In this structure, the FP (inserted in the host cell membrane) and MSR (inserted in the viral membrane) are in close proximity. ERVs are likely to originate from ancient germ-line infections by active retroviruses. Some modern ERVs, those that integrated into the host genome post-speciation, have a currently active exogenous counterpart, such as FeLV. Some ERVs play specific roles in the host, including placental development, protection of the host from infection by related pathogenic and exogenous retroviruses, and genome plasticity. Syncytin-1 and Syncytin-2 are expressed in the placenta, and are fusogenic, although they have a different cell specificity for fusion. Syncytin-2, but not Syncytin-1, is immunosuppressive; its immunosuppressive domain may protect the fetus from the mother's immune system. Syncytin-1 may participate in the formation of the placental trophoblast; it is also implicated in cell fusions between cancer and host cells and between cancer cell, and in human osteclast fusion. This subfamily also contains a mouse envelope protein encoded by the Fv-4 env gene, that blocks infection by exogenous MuLV.

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gi 221326518 475 QFEQLQAAIHTDLGALEKSVSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCFYADHTGVVRDSMAKLR 551
Cdd:cd09851    2 SYKSLSHALDADIQRLAQSISKLQKQLTSLAEVVLQNRRGLDLLTLEQGGLCAALQEECCFYANQSGLVRDSIAKLR 78

heptad repeat 1-heptad repeat 2 region (ectodomain) of the transmembrane subunit of human T-cell leukemia virus type 1 (HTLV-1), and related domains; This domain subfamily spans both heptad repeats of the glycoprotein (gp)/transmembrane(TM) subunit of various endogenous retroviruses (ERVs) and infectious retroviruses, including HTLV-1, HTLV -2, primate Mason-Pfizer monkey virus, Moloney murine leukemia virus, simian T-cell lymphotropic virus, feline leukemia virus (FeLV), bovine leukemia virus, and various human endogenous retroviruses (HERVs), including, HERV-H1_c2q24.3, HERV-H2_3q26, HERV-F(c)1_cXq21.33, HERV-T_19q13.11, Syncytin-1 (HERV-W_c7q21.2/ ERVWE1), Syncytin-2 (HERV-FRD_6p24.1), and related domains. This domain includes an N-terminal heptad repeat, a CKS17-like immunosuppressive region, a CX6C motif that forms an intrasubunit disulfide bond, and a C-terminal heptad repeat. N-terminal to HR1-HR2 region is a fusion peptide (FP), and C-terminal, is a membrane-spanning region (MSR). Viral infection involves the formation of a trimer-of-hairpins structure (three HR1s helices, buttressed by three HR2 helices lying in antiparallel orientation). In this structure, the FP (inserted in the host cell membrane) and MSR (inserted in the viral membrane) are in close proximity. ERVs are likely to originate from ancient germ-line infections by active retroviruses. Some modern ERVs, those that integrated into the host genome post-speciation, have a currently active exogenous counterpart, such as FeLV. Some ERVs play specific roles in the host, including placental development, protection of the host from infection by related pathogenic and exogenous retroviruses, and genome plasticity. Syncytin-1 and Syncytin-2 are expressed in the placenta, and are fusogenic, although they have a different cell specificity for fusion. Syncytin-2, but not Syncytin-1, is immunosuppressive; its immunosuppressive domain may protect the fetus from the mother's immune system. Syncytin-1 may participate in the formation of the placental trophoblast; it is also implicated in cell fusions between cancer and host cells and between cancer cell, and in human osteclast fusion. This subfamily also contains a mouse envelope protein encoded by the Fv-4 env gene, that blocks infection by exogenous MuLV.

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gi 221326518 475 QFEQLQAAIHTDLGALEKSVSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCFYADHTGVVRDSMAKLR 551
Cdd:cd09851    2 SYKSLSHALDADIQRLAQSISKLQKQLTSLAEVVLQNRRGLDLLTLEQGGLCAALQEECCFYANQSGLVRDSIAKLR 78

heptad repeat 1-heptad repeat 2 region (ectodomain) of the transmembrane subunit of the human endogenous retrovirus ENVV1, and related domains; This domain subfamily spans both heptad repeats of the glycoprotein (gp)/transmembrane subunit of various endogenous retroviruses (ERVs), including chicken FET-1 (Female Expressed Transcript 1) protein, and the envelope proteins of the human ERVs (HERVs): ENVV1 (also known as HERV-V2_c19q13.41) and ENVV2 (also known as HERV-V1_c19q13.41 ). This domain belongs to a larger superfamily containing the HR1-HR2 domain of endogenous retroviruses (ERVs) and infectious retroviruses, such as Ebola virus, Rous sarcoma virus and human immunodeficiency virus type 1. This domain includes an N-terminal heptad repeat, a CKS17-like immunosuppressive region, a CX6C motif that forms an intra-subunit disulfide bond, and a C-terminal heptad repeat. N-terminal to HR1-HR2 region is a fusion peptide (FP), and C-terminal, is a membrane-spanning region (MSR). Viral infection involves the formation of a trimer-of-hairpins structure (three HR1 helices, buttressed by three HR2 helices lying in antiparallel orientation). In this structure, the FP (inserted in the host cell membrane) and MSR (inserted in the viral membrane) are in close proximity. ERVs are likely to originate from ancient germ-line infections by active retroviruses. Some ERVs play specific roles in the host, including placental development, protection of the host from infection by related pathogenic and exogenous retroviruses, and genome plasticity. FET-1 may have an ovary-determining role. The FET-1 gene is located on the female specific W chromosome in chickens. During the sex-determining period, the FET-1 transcript is up-regulated in the cortex of the left gonad (the only gonad which develops in female chickens); it is also expressed at a lower level, in neural tissue and waste collection ducts. The genes encoding ENVV1 and ENVV2 proteins are located in tandem on chromosome 19q13.41, and show placenta-specific expression in human and baboon.

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gi 221326518 493 SVSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCFYADHTGVVRDSMAKLRER 553
Cdd:cd09950   12 SISALQAEVSSLSNVVLQNRMALDLLLAEQGGVCAVINQSCCAYVNNSGRIETDIKKIYDQ 72

heptad repeat 1-heptad repeat 2 region (ectodomain) of the transmembrane subunit of various endogenous retroviruses (ERVs) and infectious retroviruses, including Ebola virus and human immunodeficiency virus type 1 (HIV-1); This domain superfamily spans both heptad repeats of the glycoprotein (gp)/transmembrane subunit of various endogenous retroviruses (ERVs) and infectious retroviruses, including Ebola virus gp2, Rous sarcoma virus gp37, human immunodeficiency virus type 1 (HIV-1) gp41, and the envelope proteins of various ERVs. In the HR1-HR2 region of Ebola virus and RSV, the linker region between the two repeats includes a CKS17-like immunosuppressive region and a CX6C motif that forms an intra-subunit disulfide bond; MMTV, HIV-1, HERV-K endogenous retroviruses and related sequences lack a canonical CSK17-like sequence, and CX6C motif. N-terminal to the HR1-HR2 region is a fusion peptide (FP), and C-terminal, is a membrane-spanning region (MSR). Viral infection involves the formation of a trimer-of-hairpins structure (three HR1 helices, buttressed by three HR2 helices lying in antiparallel orientation). In this structure, the FP (inserted in the host cell membrane) and MSR (inserted in the viral membrane) are in close proximity. ERVs are likely to originate from ancient germ-line infections by active retroviruses. Some modern ERVs, those that integrated into the host genome post-speciation, have a currently active exogenous counterpart, such as Jaagsiekte sheep retrovirus (JSRV), feline leukemia virus (FeLV), and avian leukemia virus (ALV). Some ERVs play specific roles in the host, including placental development, protection of the host from infection by related pathogenic and exogenous retroviruses, and genome plasticity. Human ERVs (HERVs) belonging to this superfamily include Syncytin-1 (HERV-W_c7q21.2/ ERVWE1), and Syncytin-2 (HERV-FRD_6p24.1) which are expressed in the placenta, and are fusogenic, although they have a different cell specificity for fusion. Syncytin-2, but not Syncytin-1, is immunosuppressive; its immunosuppressive domain may protect the fetus from the mother's immune system. Syncytin-1 may participate in the formation of the placental trophoblast; it is also implicated in cell fusions between cancer and host cells and between cancer cell, and in human osteclast fusion. This superfamily also contains human HERV-R_c7q21.2 (ERV-3), which is also expressed in the placenta, but is not fusogenic, and has an immunosuppressive domain, but lacks a fusion peptide. It is unclear whether ERV-3 has a critical biological role. Included in this superfamily are ERVs from domestic sheep that are related to JSRV, the agent of transmissible lung cancer in sheep; for example, enJSRV-26 that retains an intact genome. These endogenous JSRVs protect the sheep against JSRV infection and are required for sheep placental development.

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gi 221326518 486 DLGALEKSVSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCFYA-DHTGVVRDSMAKLRER 553
Cdd:cd09947    5 LLRLTTQAIKNLHTNLTAIAKYLAQNRRGLDWLAARRGGTCVALTEVCCPFLsITNKWWQDWIRKLDFL 73

heptad repeat 1-heptad repeat 2 region (ectodomain) of the transmembrane subunit of Rous sarcoma virus (RSV), and related domains; This domain subfamily spans both heptad repeats of the glycoprotein (gp)/transmembrane subunit of various endogenous retroviruses (ERVs) and infectious retroviruses, including Rous sarcoma virus gp37, Avian leukosis virus subgroup J (ALV-J) envelope protein, and the envelope proteins of various ERVs, including those belonging to the ev/J (or EAV-HP) family of chicken ERVs, such as ev/J 4.1 Rb. ALV-J is a recently emerged avian pathogen, the causative agent of myeloid leukosis in meat-type chicken. ERVs are likely to originate from ancient germ-line infections by active retroviruses. ALV-J may have emerged from a recombination event between an unknown ALV and an EAV-HP ERV. This domain includes an N-terminal heptad repeat, a CKS17-like immunosuppressive region, a CX6C motif that forms an intrasubunit disulfide bond, and a C-terminal heptad repeat. N-terminal to HR1-HR2 region is a fusion peptide (FP), and C-terminal, is a membrane-spanning region (MSR). Viral infection involves the formation of a trimer-of-hairpins structure (three HR1s helices, buttressed by three HR2 helices lying in antiparallel orientation). In this structure, the FP (inserted in the host cell membrane) and MSR (inserted in the viral membrane) are in close proximity.

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                 ....*....|....*....|....*....|....*....|..
gi 221326518 494 VSALEKSLTSLSEVVLQNRRGLDLLFLKEGGLCAALKEECCF 535
Cdd:cd09949   13 LNDLLEDIGSIRHAVLQNRAAIDFLLLAHGHGCEDFEGLCCF 54