Human H2-T22 ORF clone (NM_010397.4)

Name: Human H2-T22 ORF clone (NM_010397.4)
SKU: CDCL115867
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CDCL115867

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Product Information

Gene Information

Cat. No.	CDCL115867
Description	Mus musculus histocompatibility 2, T region locus 22 (H2-T22), mRNA.
Product Type	ORF clone
Gene Abbr	H2-T22
Species	Mouse
ORF Size	1140bp
Format	purified plasmid
Vector	pDONR
Warning	Please note that the protein for this clone has been annotated or predicted in the UNIPROT database to have a signal peptide. Placing a tag at the N-terminus of this protein may result in loss of the signal peptide function.

Target Gene

H2-T22

Background

Predicted to enable several functions, including 14-3-3 protein binding activity; TAP binding activity; and signaling receptor binding activity. Predicted to be involved in several processes, including antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independent; antigen processing and presentation of endogenous peptide antigen via MHC class Ib; and positive regulation of T cell mediated cytotoxicity. Predicted to be located in several cellular components, including bounding membrane of organelle; cell surface; and endoplasmic reticulum. Predicted to be part of MHC class I protein complex and MHC class Ib protein complex. Predicted to be active in external side of plasma membrane and extracellular space. Is expressed in several structures, including brain; genitourinary system; gut; respiratory system; and skeleton. Human ortholog(s) of this gene implicated in several diseases, including Stevens-Johnson syndrome; asthma (multiple); autoimmune disease (multiple); eye disease (multiple); and inner ear disease (multiple). Orthologous to several human genes including HLA-B (major histocompatibility complex, class I, B); HLA-C (major histocompatibility complex, class I, C); and HLA-E (major histocompatibility complex, class I, E). [provided by Alliance of Genome Resources, Feb 2025]

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