Редактирование: AMBP

Protein AMBP precursor [Contains: Alpha-1-microglobulin (Protein HC) (Alpha-1 microglycoprotein) (Complex-forming glycoprotein heterogeneous in charge); Inter-alpha-trypsin inhibitor light chain (ITI-LC) (Bikunin) (EDC1) (HI-30) (Uronic-acid-rich protein); Trypstatin] [HCP] [ITIL]

==Publications==

{{medline-entry
|title=Developmentally regulated transcription of the four liver-specific genes for inter-alpha-inhibitor family in mouse.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/7504460
|abstract=The inter-alpha-inhibitor family is composed of the plasma-protease inhibitors inter-alpha-inhibitor, pre-alpha-inhibitor and bikunin. Inter-alpha-inhibitor and pre-alpha-inhibitor are distinct assemblies of bikunin with distinct sets from three heavy (H) chains designated H1, H2 and H3. These H chains are encoded by a set of three evolutionarily related H genes, and bikunin by an alpha-1-microglobulin/bikunin precursor gene ([[AMBP]]). This precursor is cleaved to yield bikunin, a member of the Kunitz-type protease-inhibitor superfamily, and alpha-1-microglobulin, which belongs to the lipocalin superfamily. Northern-blot experiments with RNAs obtained from various tissues in fetal and in adult mice indicated that the transcription of the four [[AMBP]] and H genes is liver-restricted, although there is expression of H3 in brain. An analysis of the H1, H2, H3 and [[AMBP]] transcripts, as well as of transcripts for other control genes, in liver during development showed a progressive increase in the amounts of the H1, H2, H3 and [[AMBP]] RNAs, which all peak transiently at day 5 after birth. This was shown by a nuclear run-on experiment to originate from a change in transcription rate. The transient and postnatal increase in transcription could be explained neither by the liver-restricted expression nor by a common origin of these four genes, nor by a perinatal requirement for many lipocalins or protease inhibitors. This suggests that all four genes are perinatally triggered at the level of similar elements in their transcriptional regulatory regions, a conclusion strengthened by the weak expression of the four genes that is seen in a mutant mouse strain (albino) that is deficient in some liver-specific transcription factors.
|mesh-terms=* Aging
* Albinism
* Alpha-Globulins
* Animals
* Animals, Newborn
* Female
* Fetus
* Gene Deletion
* Gene Expression Regulation
* Gestational Age
* Glycoproteins
* Humans
* Liver
* Macromolecular Substances
* Male
* Membrane Glycoproteins
* Mice
* Mice, Inbred BALB C
* Mice, Inbred C3H
* Mice, Inbred C57BL
* Mice, Inbred Strains
* Multigene Family
* Protein Precursors
* Rats
* Transcription, Genetic
* Trypsin Inhibitor, Kunitz Soybean
* Trypsin Inhibitors

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1137658
}}