240*576=138240 and the strange corona virus rabbit hole.
It can be divided in two parts, 138 and 240, that added together give a triangular number (378 = T27).
It is a happy number.
It is a Jordan-Polya number, since it can be written as 6! ⋅ 4! ⋅ (2!)3.
It is an interprime number because it is at equal distance from previous prime (138239) and next prime (138241).
It is a Harshad number since it is a multiple of its sum of digits (18).
It is a congruent number.
It is not an unprimeable number, because it can be changed into a prime (138241) by changing a digit.
It is a polite number, since it can be written in 7 ways as a sum of consecutive naturals, for example, 27646 + ... + 27650.
138240 is a Friedman number, since it can be written as 10*(8+2^4)^3, using all its digits and the basic arithmetic operations.
2138240 is an apocalyptic number.
]Gene ID: 138240
Chromosome 9 likely contains 800 to 900 genes that provide instructions for making proteins. These proteins perform a variety of different roles in the body
Chromosome 9q deletion is a chromosome abnormality that occurs when there is a missing (deleted) copy of genetic material on the long arm (q) of chromosome 9. The severity of the condition and the signs and symptoms depend on the size and location of the deletion and which genes are involved. Features that often occur in people with chromosome 9q deletion include developmental delay, intellectual disability, behavioral problems and distinctive facial features.[1][2] Chromosome testing of both parents can provide more information on whether or not the deletion was inherited. In most cases, parents do not have any chromosomal anomaly. However, sometimes one parent is found to have a balanced translocation, where a piece of a chromosome has broken off and attached to another one with no gain or loss of genetic material. The balanced translocation normally does not cause any signs or symptoms, but it increases the risk for having an affected child with a chromosomal anomaly like a deletion. Treatment is based on the signs and symptoms present in each person.
The following chromosomal conditions are associated with changes in the structure or number of copies of chromosome 9.
9q22.3 microdeletion is a chromosomal change in which a small piece of the long (q) arm of chromosome 9 is deleted in each cell. Affected individuals are missing at least 352,000 base pairs, also written as 352 kilobases (kb), in the q22.3 region of chromosome 9. This 352-kb segment is known as the minimum critical region because it is the smallest deletion that has been found to cause the signs and symptoms related to 9q22.3 microdeletions. These signs and symptoms include delayed development, intellectual disability, certain physical abnormalities, and the characteristic features of a genetic condition called Gorlin syndrome (also known as nevoid basal cell carcinoma syndrome). 9q22.3 microdeletions can also be much larger; the largest reported deletion included 20.5 million base pairs (20.5 Mb).
People with a 9q22.3 microdeletion are missing two to more than 270 genes on chromosome 9. All known 9q22.3 microdeletions include the PTCH1 gene. Researchers believe that many of the features associated with 9q22.3 microdeletions, particularly the signs and symptoms of Gorlin syndrome, result from a loss of the PTCH1 gene. Other signs and symptoms related to 9q22.3 microdeletions probably result from the loss of additional genes in the q22.3 region. Researchers are working to determine which missing genes contribute to the other features associated with the deletion.
Deletions of part or all of chromosome 9 are commonly found in bladder cancers. These chromosomal changes are seen only in cancer cells and typically occur early in tumor formation. Researchers believe that several genes that play a role in bladder cancer may be located on chromosome 9. They suspect that these genes may be tumor suppressors, which means they normally help prevent cells from growing and dividing in an uncontrolled way. Researchers are working to determine which genes, when altered or missing, are involved in the development and progression of bladder tumors.
A rearrangement (translocation) of genetic material between chromosomes 9 and 22 causes a type of cancer of blood-forming cells called chronic myeloid leukemia. This slow-growing cancer leads to an overproduction of abnormal white blood cells. Common features of the condition include excessive tiredness (fatigue), fever, weight loss, and an enlarged spleen.
The translocation involved in this condition, written as t(9;22), fuses part of the ABL1 gene from chromosome 9 with part of the BCR gene from chromosome 22, creating an abnormal fusion gene called BCR-ABL1. The abnormal chromosome 22, containing a piece of chromosome 9 and the fusion gene, is commonly called the Philadelphia chromosome. The translocation is acquired during a person's lifetime and is present only in the abnormal blood cells. This type of genetic change, called a somatic mutation, is not inherited.
The protein produced from BCR-ABL1 gene signals cells to continue dividing abnormally and prevents them from self-destructing, which leads to overproduction of the abnormal cells.
The Philadelphia chromosome also has been found in some cases of rapidly progressing blood cancers known as acute leukemias. It is likely that the form of blood cancer that develops is influenced by the type of blood cell that acquires the mutation and other genetic changes that occur. The presence of the Philadelphia chromosome provides a target for molecular therapies.
Most people with Kleefstra syndrome, a disorder with signs and symptoms involving many parts of the body, are missing a sequence of about 1 million DNA building blocks (base pairs) on one copy of chromosome 9 in each cell. The deletion occurs near the end of the long (q) arm of the chromosome at a location designated q34.3, a region containing a gene called EHMT1. Some affected individuals have shorter or longer deletions in the same region.
The loss of the EHMT1 gene from one copy of chromosome 9 in each cell is believed to be responsible for the characteristic features of Kleefstra syndrome in people with the 9q34.3 deletion. However, the loss of other genes in the same region may lead to additional health problems in some affected individuals.
The EHMT1 gene provides instructions for making an enzyme called euchromatic histone methyltransferase 1. Histone methyltransferases are enzymes that modify proteins called histones. Histones are structural proteins that attach (bind) to DNA and give chromosomes their shape. By adding a molecule called a methyl group to histones, histone methyltransferases can turn off (suppress) the activity of certain genes, which is essential for normal development and function. A lack of euchromatic histone methyltransferase 1 enzyme impairs proper control of the activity of certain genes in many of the body's organs and tissues, resulting in the abnormalities of development and function characteristic of Kleefstra syndrome.
Changes in the structure of chromosome 9 have been found in many types of cancer. These changes, which occur only in cells that give rise to cancer, usually involve a loss of part of the chromosome or a rearrangement of chromosomal material. For example, a loss of part of the long (q) arm of chromosome 9 has been identified in some types of brain tumor. In addition, chromosomal rearrangements that fuse the ABL1 gene with genes other than BCR have been found in a small number of acute leukemias. The exact mechanisms by which these genetic changes lead to cancer are not completely understood, although it is likely that the proteins produced from them promote uncontrolled growth of cells.
Other changes in the structure or number of copies of chromosome 9 can have a variety of effects. Intellectual disability, delayed development, distinctive facial features, and an unusual head shape are common features. Changes to chromosome 9 include an extra piece of the chromosome in each cell (partial trisomy), a missing segment of the chromosome in each cell (partial monosomy), and a circular structure called a ring chromosome 9. A ring chromosome occurs when both ends of a broken chromosome are reunited. Rearrangements (translocations) of genetic material between chromosome 9 and other chromosomes can also lead to extra or missing chromosome segments.C9orf57 chromosome 9 open reading frame 57 [ Homo sapiens (human) ]Gene ID: 138240, updated on 22-Jan-2020
Official SymbolC9orf57provided by HGNCOfficial Full Namechromosome 9 open reading frame 57provided by HGNCPrimary sourceHGNC:HGNC:27037See relatedEnsembl:ENSG00000204669Gene typeprotein codingRefSeq statusVALIDATEDOrganismHomo sapiensLineageEukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; HomoExpressionRestricted expression toward testis (RPKM 8.9) See moreOrthologsall
See C9orf57 in Genome Data ViewerLocation: 9q21.13Exon count: 5
Annotation releaseStatusAssemblyChrLocation109.20191205 current GRCh38.p13 (GCF_000001405.39) 9 NC_000009.12 (72051376..72060613, complement)
105 previous assembly GRCh37.p13 (GCF_000001405.25) 9 NC_000009.11 (74666275..74687728, complement)
Chromosome 9 - NC_000009.12
Genomic Sequence:
NC_000009.12
Find:
Clinical, dbSNP b153 v2
Warning: No track data found in this range
Cited Variations, dbSNP b153 v2
Warning: No track data found in this range
Biological regions, aggregate, NCBI Homo sapiens Annotation Release 109.20191205
Warning: No track data found in this range
Genes, Ensembl release 99
RNA-seq intron-spanning reads, aggregate (filtered), NCBI Homo sapiens Annotation Release 109 - log base 2 scaled
RNA-seq intron features, aggregate (filtered), NCBI Homo sapiens Annotation Release 109
RNA-seq exon coverage, aggregate (filtered), NCBI Homo sapiens Annotation Release 109 - log base 2 scaled
Genes, NCBI Homo sapiens Annotation Release 109.20191205
Live RefSNPs, dbSNP b153 v2
NC_000009.12: 72M..72M (12,010 nt) C
Tracks shown: 10/737
Project title: HPA RNA-seq normal tissues
Description: RNA-seq was performed of tissue samples from 95 human individuals representing 27 different tissues in order to determine tissue-specificity of all protein-coding genes
BioProject: PRJEB4337
Publication: PMID 24309898
Analysis date: Wed Apr 4 07:08:55 2018
adrenalappendixbone marrowbraincolonduodenumendometriumesophagusfatgall bladderheartkidneyliverlunglymph nodeovarypancreasplacentaprostatesalivary glandskinsmall intestinespleenstomachtestisthyroidurinary bladder024681012SamplesRPKM
DNA sequence and analysis of human chromosome 9.Humphray SJ, et al. Nature, 2004 May 27. PMID 15164053, Free PMC Article
The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).Gerhard DS, et al. Genome Res, 2004 Oct. PMID 15489334, Free PMC Article
Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.Strausberg RL, et al. Proc Natl Acad Sci U S A, 2002 Dec 24. PMID 12477932, Free PMC Article
Submit: New GeneRIF Correction
Orthologs from Annotation Pipeline: 73 organisms have orthologs with human gene C9orf57
ComponentEvidence CodePubsintegral component of membrane IEA
Preferred Namesuncharacterized protein C9orf57
These reference sequences exist independently of genome builds. Explain
mRNA and Protein(s)
NM_001128618.2 → NP_001122090.2 uncharacterized protein C9orf57 isoform 1
Status: VALIDATEDSource sequence(s)AL138751Consensus CDSCCDS47980.1RelatedENSP00000498279.1, ENST00000651200.2
NM_001371610.1 → NP_001358539.1 uncharacterized protein C9orf57 isoform 2
The following sections contain reference sequences that belong to a specific genome build. Explain
Reference GRCh38.p13 Primary Assembly
Genomic
NC_000009.12 Reference GRCh38.p13 Primary AssemblyRange72051376..72060613 complementDownloadGenBank, FASTA, Sequence Viewer (Graphics)
NucleotideProtein
HeadingAccession and Versiongenomic AL138751.18 (179273..188510) None
genomic AL583829.7 (2001..6773) None
genomic CH471089.1 EAW62527.1
mRNA BC036255.1 None
mRNA BC044620.1 None
mRNA BC053956.1 None
mRNA BC130404.1 AAI30405.1
mRNA BC144273.1 AAI44274.1
Protein AccessionLinks
GenPept LinkUniProtKB LinkQ5W0N0.1 GenPept UniProtKB/Swiss-Prot:Q5W0N0
138240 is a gapful number since it is divisible by the number (10) formed by its first and last digit.
It is an amenable number.
It is a practical number, because each smaller number is the sum of distinct divisors of 138240, and also a Zumkeller number, because its divisors can be partitioned in two sets with the same sum (245640).
138240 is an abundant number, since it is smaller than the sum of its proper divisors (353040).
It is a pseudoperfect number, because it is the sum of a subset of its proper divisors.
138240 is an equidigital number, since it uses as much as digits as its factorization.
138240 is an evil number, because the sum of its binary digits is even.
The square root of 138240 is about 371.8064012359. The cubic root of 138240 is about 51.7064325608.
N nucleocapsid protein [ Severe acute respiratory syndrome-related coronavirus ]Gene ID: 1489678, updated on 2-May-2019
Gene symbolNGene descriptionnucleocapsid proteinLocus tagsars9aGene typeprotein codingRefSeq statusREVIEWEDOrganismSevere acute respiratory syndrome-related coronavirus (isolate: Tor2)LineageViruses; Riboviria; Nidovirales; Cornidovirineae; Coronaviridae; Orthocoronavirinae; Betacoronavirus; Sarbecovirus
Sequence: NC_004718.3 (28120..29388)
NC_004718.3
Genomic Sequence: NC_004718.3
NC_004718.3
Find:
Tools
TracksDownload
5'UTR Features
Warning: No track data found in this range
region Features
Warning: No track data found in this range
misc_feature Features
3'UTR Features
Genes
NC_004718.3: 28K..30K (1,649 nt)
Tracks shown: 6/9
Transient oligomerization of the SARS-CoV N protein--implication for virus ribonucleoprotein packaging.Chang CK, et al. PLoS One, 2013. PMID 23717688, Free PMC Article
The SR-rich motif in SARS-CoV nucleocapsid protein is important for virus replication.Tylor S, et al. Can J Microbiol, 2009 Mar. PMID 19370068
Thermostability of the N-terminal RNA-binding domain of the SARS-CoV nucleocapsid protein: experiments and numerical simulations.Fang HJ, et al. Biophys J, 2009 Mar 4. PMID 19254548, Free PMC Article
Multiple nucleic acid binding sites and intrinsic disorder of severe acute respiratory syndrome coronavirus nucleocapsid protein: implications for ribonucleocapsid protein packaging.Chang CK, et al. J Virol, 2009 Mar. PMID 19052082, Free PMC Article
Prior immunization with severe acute respiratory syndrome (SARS)-associated coronavirus (SARS-CoV) nucleocapsid protein causes severe pneumonia in mice infected with SARS-CoV.Yasui F, et al. J Immunol, 2008 Nov 1. PMID 18941225
ProductsInteractantOther GeneComplexSourcePubsDescriptionNP_828858.1 NP_828858.1 N BIND PubMed Nucleocapsid protein interacts with nucleocapsid protein.
Preferred Namesnucleocapsid proteinNP_828858.1
As established by Krokhin et al. (2003), the N-terminal methionine is removed, all other methionines are oxidized, and the resulting N-terminal serine is acetylated
The following sections contain reference sequences that belong to a specific genome build. Explain
Reference assembly
Genomic
mRNA and Protein(s)
NP_828858.1 nucleocapsid protein [Severe acute respiratory syndrome-related coronavirus]
Status: REVIEWEDUniProtKB/Swiss-ProtP59595UniProtKB/TrEMBLQ19QW0, Q6S8E1Conserved Domains (1) summarypfam00937
Location:15 → 365Corona_nucleoca; Coronavirus nucleocapsid protein
NucleotideProtein
HeadingAccession and Versiongenomic AY274119.3 AAP41047.1
genomic DQ497008.1 ABF65846.1
genomic DQ898174.1 ABI96968.1
genomic JX163923.1 AFR58681.1
genomic JX163924.1 AFR58695.1
genomic JX163925.1 AFR58709.1
genomic JX163926.1 AFR58723.1
genomic JX163927.1 AFR58737.1
genomic JX163928.1 AFR58751.1
Protein AccessionLinks
GenPept LinkUniProtKB LinkP59595.1
Gene(s) Matching your query...
DISEASE OUTBREAK
Sequence data to support research and public health activities directed at the ongoing novel coronavirus (Wuhan coronavirus) outbreak. Find more outbreak information from the CDC
Search results
Items: 13
Name/Gene IDDescriptionLocationAliases
Select item 1489668
SID: 1489668 E2 glycoprotein precursor [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (21492..25259) sars2, E2
Select item 1489678
NID: 1489678 nucleocapsid protein [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (28120..29388) sars9a
Select item 1489680
orf1abID: 1489680 orf1a polyprotein (pp1a);orf1ab polyprotein (pp1ab) [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (265..21485) sars1
Select item 1489671
EID: 1489671 protein E [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (26117..26347) sars4
Select item 1489669
sars3aID: 1489669 hypothetical protein sars3a [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (25268..26092) sars3a
Select item 1489672
MID: 1489672 matrix protein [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (26398..27063) sars5
Select item 1489674
sars7aID: 1489674 hypothetical protein sars7a [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (27273..27641) sars7a
Select item 1489679
sars9bID: 1489679 hypothetical protein sars9b [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (28130..28426) sars9b
Select item 1489673
sars6ID: 1489673 hypothetical protein sars6 [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (26913..27265) sars6
Select item 1489675
sars7bID: 1489675 hypothetical protein sars7b [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (27638..27772) sars7b
Select item 1489677
sars8bID: 1489677 hypothetical protein sars8b [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (27864..28118) sars8b
Select item 1489676
sars8aID: 1489676 hypothetical protein sars8a [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (27779..27898) sars8a
Select item 1489670
sars3bID: 1489670 hypothetical protein sars3b [Severe acute respiratory syndrome-related coronavirus] NC_004718.3 (25689..26153) sars3b
