SitesBLAST

O35826 Bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase; UDP-GlcNAc-2-epimerase/ManAc kinase; EC 3.2.1.183; EC 2.7.1.60 from Rattus norvegicus (Rat) (see paper)
26% identity, 89% coverage: 10:241/260 of query aligns to 410:635/722 of O35826

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O35826

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D413 (= D13) mutation D->K,N: No effect on UDP-N-acetylglucosamine 2-epimerase activity. Does not affect feedback inhibition by CMP-Neu5Ac. Loss of N-acylmannosamine kinase activity. Does not interfere with oligomerization.
R420 (≠ K20) mutation to M: No effect on UDP-N-acetylglucosamine 2-epimerase activity. Does not affect feedback inhibition by CMP-Neu5Ac. Loss of N-acylmannosamine kinase activity. Does not interfere with oligomerization.

Sites not aligning to the query:

1 UDP-N-acetylglucosamine 2-epimerase
49 H→A: Loss UDP-N-acetylglucosamine 2-epimerase activity. No effect on N-acylmannosamine kinase activity. Does not interfere with enzyme oligomerization.
110 H→A: Loss UDP-N-acetylglucosamine 2-epimerase activity. No effect on N-acylmannosamine kinase activity. Partial reduction of the dimerization process.
132 H→A: Loss UDP-N-acetylglucosamine 2-epimerase activity. No effect on N-acylmannosamine kinase activity. Partial reduction of the dimerization process.
155 H→A: Loss UDP-N-acetylglucosamine 2-epimerase activity. No effect on N-acylmannosamine kinase activity. Strong reduction of the dimerization process.
157 H→A: Loss UDP-N-acetylglucosamine 2-epimerase activity. No effect on N-acylmannosamine kinase activity. Strong reduction of the dimerization process.
406:722 N-acetylmannosamine kinase

Q91WG8 Bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase; UDP-GlcNAc-2-epimerase/ManAc kinase; EC 3.2.1.183; EC 2.7.1.60 from Mus musculus (Mouse) (see paper)
26% identity, 89% coverage: 10:241/260 of query aligns to 410:635/722 of Q91WG8

query
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Q91WG8

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C563 (≠ P157) mutation to Y: Loss-of-function mutant resulting in impaired sialic acid biosynthesis.

Sites not aligning to the query:

704 P→R: Homozygous embryos exhibit cerebrospinal hemorrhages and defective angiogenesis in the diencephalon at 11 dpc, and become non-viable between 11.5 and 12.5 dpc. Loss-of-function mutant resulting in impaired sialic acid biosynthesis.

Query Sequence

>WP_017616663.1 NCBI__GCF_002263495.1:WP_017616663.1
MKGHAPRVGLGIDIGGSGIKGAPVDLDSGTFVVDRVKVATPQPATREAVAKVLAEIAASF
PEQVSADCPLGVTFPAVVQHGVAYSAANVDDSWVGANLEHVFSEVTGRRVHVLNDADAAA
VAEHRYGAARDAEGVVLLTTLGTGIGTALLVDGRLVPNTEFGHLEIDGHDAESRAASSAR
EREDLSYEEWATQRLQRYYSVVEDLLSPDLIVVGGGVSRKADRFLPLLHLRAPILAARLR
NTAGIVGAAVAAAERFGAPS

Or try a new SitesBLAST search

SitesBLAST's Database

SitesBLAST's database includes (1) SwissProt entries with experimentally-supported functional features; and (2) protein structures with bound ligands, from the BioLip database.

by Morgan Price, Arkin group
Lawrence Berkeley National Laboratory