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ANXA7 Knockout Cell Lines

Gene: ANXA7

Official Full Name: annexin A7provided by HGNC

Gene Summary: Annexin VII is a member of the annexin family of calcium-dependent phospholipid binding proteins.The Annexin VII gene contains 14 exons and spans approximately 34 kb of DNA. An alternatively spliced cassette exon results in two mRNA transcripts of 2.0 and 2.4 kb which are predicted to generate two protein isoforms differing in their N-terminal domain. The alternative splicing event is tissue specific and the mRNA containing the cassette exon is prevalent in brain, heart and skeletal muscle. The transcripts also differ in their 3'-non coding regions by the use of two alternative poly(A) signals. Annexin VII encodes a protein with a molecular weight of approximately 51 kDa with a unique, highly hydrophobic N-terminal domain of 167 amino acids and a conserved C-terminal region of 299 amino acids. The latter domain is composed of alternating hydrophobic and hydrophilic segments. Structural analysis of the protein suggests that Annexin VII is a membrane binding protein with diverse properties, including voltage-sensitive calcium channel activity, ion selectivity and membrane fusion. [provided by RefSeq, Jul 2008]

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Products Background

Products

Catalog Number Product Name Species Gene Passage ratio Mycoplasma testing Price
KO38997 ANXA7 Knockout cell line (HeLa) Human ANXA7 1:3~1:6 Negative Online Inquiry
KO38998 ANXA7 Knockout cell line (HCT 116) Human ANXA7 1:2~1:4 Negative Online Inquiry
KO38999 ANXA7 Knockout cell line (HEK293) Human ANXA7 1:3~1:6 Negative Online Inquiry
KO39000 ANXA7 Knockout cell line (A549) Human ANXA7 1:3~1:4 Negative Online Inquiry

Background

ANXA7 Gene Knockout Cell Lines are innovative cellular models engineered to lack the expression of the annexin A7 (ANXA7) protein, which plays a pivotal role in various cellular processes including calcium signaling, membrane trafficking, and apoptosis. These knockout cell lines facilitate profound insights into the functional significance of ANXA7 in health and disease states by providing a precise platform for experimental manipulation.

The production of ANXA7 knockout cells employs CRISPR/Cas9 technology, a cutting-edge genome editing tool that allows for targeted disruption of the ANXA7 gene. Consequently, these cell lines serve as exceptional resources for elucidating the mechanisms by which ANXA7 influences cellular behavior and interacts with other molecular pathways. Researchers can utilize these lines to investigate the implications of ANXA7 deficiency in diseases such as cancer, neurodegenerative disorders, and cardiac pathologies, where its involvement may be critical.

The scientific importance of ANXA7 knockout cell lines extends to their utility in both basic research and clinical settings. Investigators can leverage these models to explore novel therapeutic targets, develop drug screening assays, and characterize cellular responses to various stimuli in a controlled environment. In contrast to traditional wild-type cell lines, the ability to study gene function in the absence of ANXA7 allows for clearer insights into its role and the potential implications for human health.

Additionally, these knockout cell lines offer distinct advantages over alternatives in terms of specificity and reproducibility. While conventional methods may provide less definitive conclusions through pharmacological inhibition or knockdown approaches, the complete gene knockout ensures that any phenotypic changes observed can be directly attributed to the absence of ANXA7.

In summary, ANXA7 Gene Knockout Cell Lines are invaluable tools for researchers aiming to deepen their understanding of cellular processes and disease mechanisms associated with the ANXA7 protein. By choosing our product, users gain access to state-of-the-art biological models backed by our company’s expertise in genetic engineering and commitment to advancing research through high-quality biological products.

Please note that all services are for research use only. Not intended for any clinical use.

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